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PubMed: 29956069

Title
Mechanisms of Hemolysis During Sepsis.
Journal
Inflammation
Volume
41
Issue
None
Pages
1569-1581
Date
2018-10-01
Authors
Effenberger-Neidnicht K | Hartmann M

Evidence 7859c0a72a
JSON

Another pathogenic mechanism involves the release of iron from cell-free hemoglobin with consecutive radical formation, which in turn can modify lipids, proteins, and DNA, leading to inflammation [39].

a(CHEBI:"iron(2+)") increases bp(GO:"inflammatory response") View Subject | View Object

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Arteries
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Sepsis
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p(HGNC:HBB) increases a(CHEBI:"iron(2+)") View Subject | View Object

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Evidence 21377b888e
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Lipid A alone, however, does not appear to affect the osmotic resistance of red blood cells [127].

a(CHEBI:"lipid A") causesNoChange bp(MESH:"Osmotic Fragility") View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
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Evidence d40e6115a7
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Hemodynamics will be impaired, which on the one hand can lead to the production of oxygen radicals and thus directly to tissue damage.

a(CHEBI:"oxygen radical") positiveCorrelation path(MESH:Sepsis) View Subject | View Object

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Sepsis
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a(CHEBI:"oxygen radical") directlyIncreases path(HP:"cell and tissue damage") View Subject | View Object

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Arteries
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Sepsis
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path(MESH:Sepsis) positiveCorrelation a(CHEBI:"oxygen radical") View Subject | View Object

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Arteries
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Sepsis
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Evidence 8c2058216b
JSON

However, 6 years later, Heyes and co-workers demonstrated in an experimental study in rats that infusions of thrombin induce DIC accompanied with hemolysis and schistocytosis [89].

a(CHEBI:Thrombin) positiveCorrelation path(MESH:"Disseminated Intravascular Coagulation") View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Adenocarcinoma
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a(CHEBI:Thrombin) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Adenocarcinoma
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a(CHEBI:Thrombin) positiveCorrelation a(HM:schistocytosis) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Adenocarcinoma
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a(HM:schistocytosis) positiveCorrelation a(CHEBI:Thrombin) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Adenocarcinoma
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path(MESH:"Disseminated Intravascular Coagulation") positiveCorrelation a(CHEBI:Thrombin) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Adenocarcinoma
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path(MESH:Hemolysis) positiveCorrelation a(CHEBI:Thrombin) View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Adenocarcinoma
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Evidence 31de443f8c
JSON

Recently, using a rat model of lipopolysaccharide (LPS)-induced systemic inflammation, our own collaboration could show that argatroban (a specific direct thrombin inhibitor and consequently an inhibitor of coagulation) abolishes DIC, schistocyte formation, and hemolysis.

a(CHEBI:argatroban) decreases path(MESH:"Disseminated Intravascular Coagulation") View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
Text Location
Review

a(CHEBI:argatroban) decreases a(HM:schistocytosis) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
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Review

a(CHEBI:argatroban) decreases path(MESH:Hemolysis) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
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Review

Evidence 726d0f2629
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Eryptosis is tightly regulated and triggered by a wide range of (endogenous) mediators and stimuli such as calcium signaling, ceramide formation, complement activation, energy depletion, eicosanoid release, hemolysin, and heme [140–142].

a(CHEBI:ceramide) increases bp(MESH:Eryptosis) View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

a(CHEBI:heme) increases bp(MESH:Eryptosis) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

a(MESH:Eicosanoids) increases bp(MESH:Eryptosis) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

bp(GO:"complement activation") increases bp(MESH:Eryptosis) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

bp(MESH:"Calcium Signaling") increases bp(MESH:Eryptosis) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

p(PFAM:Leukocidin) increases bp(MESH:Eryptosis) View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

Evidence e60b311c50
JSON

Interestingly, inhibition of coagulation is capable of diminishing DIC and hemolysis but not antiplatelet therapy—treatment with eptifibatide (an antiplatelet drug of the glycoprotein IIb/IIIa inhibitor class) failed to reduce LPS-induced DIC, schistocyte formation, and hemolysis.

a(CHEBI:eptifibatide) causesNoChange path(MESH:"Disseminated Intravascular Coagulation") View Subject | View Object

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
Text Location
Review

a(CHEBI:eptifibatide) causesNoChange a(HM:schistocytosis) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
Text Location
Review

a(CHEBI:eptifibatide) causesNoChange path(MESH:Hemolysis) View Subject | View Object

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
Text Location
Review

Evidence 1244624422
JSON

Without sufficient glucose supply, red blood cells will starve and perish and cytoplasmic components will release. Hemolysis will be the consequence [120].

a(CHEBI:glucose) negativeCorrelation path(MESH:Hemolysis) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Disseminated Intravascular Coagulation
Text Location
Review

path(MESH:Hemolysis) negativeCorrelation a(CHEBI:glucose) View Subject | View Object

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Disseminated Intravascular Coagulation
Text Location
Review

Evidence a682b1ef6a
JSON

Recently, our own collaboration could show that moderate glucose supply reduces hemolysis in rats treated with LPS to induce systemic inflammation [121].

a(CHEBI:glucose) negativeCorrelation path(MESH:Hemolysis) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Disseminated Intravascular Coagulation
Text Location
Review

path(MESH:Hemolysis) negativeCorrelation a(CHEBI:glucose) View Subject | View Object

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Disseminated Intravascular Coagulation
Text Location
Review

Evidence c2fa336ac0
JSON

In infectious diseases, such as malaria and sepsis, high amounts of cell-free hemoglobin and heme were found [8], suggesting that hemolysis during sepsis and systemic inflammation is of pathophysiological relevance.

a(CHEBI:heme) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Appears in Networks:
Annotations
Cell Ontology (CL)
hepatocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

a(CHEBI:heme) positiveCorrelation path(MESH:Inflammation) View Subject | View Object

Appears in Networks:
Annotations
Cell Ontology (CL)
hepatocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

p(HGNC:HBB) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Appears in Networks:
Annotations
Cell Ontology (CL)
hepatocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

p(HGNC:HBB) positiveCorrelation path(MESH:Inflammation) View Subject | View Object

Appears in Networks:
Annotations
Cell Ontology (CL)
hepatocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation p(HGNC:HBB) View Subject | View Object

Appears in Networks:
Annotations
Cell Ontology (CL)
hepatocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation a(CHEBI:heme) View Subject | View Object

Appears in Networks:
Annotations
Cell Ontology (CL)
hepatocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

path(MESH:Inflammation) positiveCorrelation a(CHEBI:heme) View Subject | View Object

Appears in Networks:
Annotations
Cell Ontology (CL)
hepatocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

path(MESH:Inflammation) positiveCorrelation p(HGNC:HBB) View Subject | View Object

Appears in Networks:
Annotations
Cell Ontology (CL)
hepatocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

Evidence dc49e54d8d
JSON

Heme released from cell-free hemoglobin has been described to be an activator of TLR-4 [39, 41, 42].

a(CHEBI:heme) increases p(HGNC:TLR4) View Subject | View Object

Appears in Networks:
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Arteries
MeSH
Sepsis
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Review

Evidence 26f39c3428
JSON

Heme/TLR-4 signaling, moreover, was found to activate NF-κB and trigger vaso-occlusion [42].

a(CHEBI:heme) increases p(HGNC:TLR4) View Subject | View Object

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Arteries
MeSH
Sepsis
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Review

a(CHEBI:heme) increases path(HM:"vaso-occlusive crisis") View Subject | View Object

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MeSH
Arteries
MeSH
Sepsis
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Review

a(CHEBI:heme) increases p(HGNC:NFKB1) View Subject | View Object

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Arteries
MeSH
Sepsis
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Evidence 858200b69b
JSON

Cell-free hemoglobin and its prosthetic group heme can contribute to organ dysfunction and death [1–4, 9–12]; the pathological mechanisms include nitric oxide consumption, vasoconstriction, oxidative injury to lipid membranes, activation of the transcription factor NF-κB, endothelial injury as well as iron-driven oxidative inhibition of glucose metabolism[10–14].

a(CHEBI:heme) increases bp(MESH:"Oxidative Stress") View Subject | View Object

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a(CHEBI:heme) increases bp(GO:"nitric oxide storage") View Subject | View Object

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a(CHEBI:heme) increases bp(GO:vasoconstriction) View Subject | View Object

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a(CHEBI:heme) increases p(HGNC:NFKB1) View Subject | View Object

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a(CHEBI:heme) decreases bp(HP:"glucose metabolic process") View Subject | View Object

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Evidence c9bb0950d0
JSON

Already in 1941, Macfarlane and collaborators described hemolysis due to loss of lecithin from the red blood cell membrane in consequence of an infection with Clostridium perfingens [128, 130].

a(CHEBI:lecithin) negativeCorrelation path(MESH:Hemolysis) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

path(MESH:Hemolysis) negativeCorrelation a(CHEBI:lecithin) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

Evidence 510c125146
JSON

In animal experiments, the administration of lipopolysaccharide (LPS) to induce systemic inflammation leads to a significant increase in plasma concentration of cell-free hemoglobin as well [5–8].

a(CHEBI:lipopolysaccharide) increases p(HGNC:HBB) View Subject | View Object

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Evidence cb06dd875e
JSON

Due to these properties, LPS can easily be incorporated into the membrane of (red blood) cells, alter their membrane properties, and thus promote cell death [123, 124].

a(CHEBI:lipopolysaccharide) increases bp(GO:"cell death") View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

Evidence c05cd9fb64
JSON

We found, moreover, a decreased osmotic resistance and membrane stiffness of washed red blood cells treated with LPS [80, 81].

a(CHEBI:lipopolysaccharide) increases bp(MESH:"Osmotic Fragility") View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

Evidence 45a0b256bc
JSON

One crucial factor in pathogenesis of systemic inflammation/sepsis is an impaired microcirculation [99].

a(HM:"Impaired microcirculation") positiveCorrelation path(MESH:Sepsis) View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
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Review

path(MESH:Sepsis) positiveCorrelation a(HM:"Impaired microcirculation") View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
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Review

Evidence 603b0d9057
JSON

The cause of sepsis is primarily an exaggerated, generalized inflammatory response to an extrinsic stimulus. Mechanistically, so-called PAMPs (pathogen-associated molecular patterns) lead to the activation of pattern recognition receptors (PRRs) such as tolllike receptors (TLRs) and C-type lectin receptors (CLRs) [28, 29].

a(HM:"Pathogen Associated Molecular Pattern") increases act(p(HGNC:TLR4)) View Subject | View Object

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Sepsis
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a(HM:"Pathogen Associated Molecular Pattern") increases act(p(PFAM:"Lectin_C")) View Subject | View Object

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MeSH
Sepsis
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Review

Evidence 2922fa5118
JSON

This study further supports the concept that fibrin deposition in the blood vessels as a result of DIC might contribute to red blood cell fragmentation and, in turn, hemolysis [89].

a(HM:"fibrin deposition") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
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Review

path(MESH:Hemolysis) positiveCorrelation a(HM:"fibrin deposition") View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
Text Location
Review

Evidence b8d899d06a
JSON

Moreover, longer storage duration of red blood cells is associated with an increased risk of acute lung injury in patients with sepsis [63].

a(HM:"stored erythrocytes") positiveCorrelation path(MESH:"Acute Lung Injury") View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
hepatocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

path(MESH:"Acute Lung Injury") positiveCorrelation a(HM:"stored erythrocytes") View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
hepatocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

Evidence ab36e412bf
JSON

Some pathogens are capable of causing hemolysis by cytolytic toxins.

a(HM:cytolysin) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation a(HM:cytolysin) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

Evidence c3e212b406
JSON

During DIC, fibrin strands within the fibrin mesh formed could cut red blood cells, resulting in the formation of schistocytes (strongly deformed red blood cells or fragments of red blood cells) and the release of hemoglobin.

a(HM:schistocytes) positiveCorrelation a(MESH:Fibrin) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
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Review

a(MESH:Fibrin) positiveCorrelation a(HM:schistocytes) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
Text Location
Review

a(MESH:Fibrin) positiveCorrelation p(HGNC:HBB) View Subject | View Object

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
Text Location
Review

p(HGNC:HBB) positiveCorrelation a(MESH:Fibrin) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
Text Location
Review

Evidence c42dadde81
JSON

Essential for the development of DIC during sepsis is the so-called pro-coagulatory shift of the endothelial cells, caused among others by an increased expression of tissue factor and adhesion molecules especially by damaged endothelial cells [87].

a(MESH:"Cell Adhesion Molecules") increases path(MESH:"Disseminated Intravascular Coagulation") View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Sepsis
Text Location
Review

p(HGNC:F3) increases path(MESH:"Disseminated Intravascular Coagulation") View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Sepsis
Text Location
Review

Evidence 74786d061c
JSON

However, also the anaphylatoxins C3a and C5a may lead to cellular and organ disturbances [75].

a(MESH:"Complement C3a") increases path(MESH:Hemolysis) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

a(MESH:"Complement C5a") increases path(MESH:Hemolysis) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

Evidence 4b3db9729d
JSON

Ultimately, activation of the complement cascade results in formation of the terminal complement complex C5b-9, the so-called membrane attack complex, and consequently a pore formation resulting in osmotic lysis of the target [71]. In the case of red blood cells, hemolysis will result.

a(MESH:"Complement Membrane Attack Complex") increases path(MESH:Hemolysis) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Hemolysis
Text Location
Review

a(MESH:"Complement Membrane Attack Complex") increases bp(GO:cytolysis) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Hemolysis
Text Location
Review

Evidence e833a411e6
JSON

During extravascular hemolysis, the IgG-coated red blood cells are degraded in the so-called reticuloendothelial systems such as liver, spleen, and lymph nodes.

a(MESH:"Lymph Nodes") increases deg(complex(GO:"IgG immunoglobulin complex")) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Hemolysis
Text Location
Review

a(MESH:Liver) increases deg(complex(GO:"IgG immunoglobulin complex")) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Hemolysis
Text Location
Review

a(MESH:Spleen) increases deg(complex(GO:"IgG immunoglobulin complex")) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Hemolysis
Text Location
Review

Evidence 1b7bad2d99
JSON

The earliest documented effect of PFTs is their ability to rapidly kill red blood cells through osmotic lysis.

a(MESH:"Pore Forming Cytotoxic Proteins") increases bp(GO:cytolysis) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

Evidence b4286cb755
JSON

In recent years, it has also been shown that toll-like receptors and other pattern recognition receptors are activated not only by extrinsic factors but also by intrinsic stimuli (so called damage-associated molecular patterns, DAMPs) that are released when the host cell is damaged [27, 29].

a(MESH:Alarmins) increases act(p(HGNC:TLR4)) View Subject | View Object

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MeSH
Arteries
MeSH
Sepsis
Text Location
Review

Evidence 1ffc7cddc2
JSON

The cytokines released can further lead to pronounced peripheral vasodilation with arterial hypotension by activating the inducible nitric oxide (NO) synthase (iNOS) and the subsequent formation of NO [30].

a(MESH:Cytokines) increases bp(GO:vasodilation) View Subject | View Object

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MeSH
Arteries
MeSH
Sepsis
Text Location
Review

a(MESH:Cytokines) increases path(MESH:Hypotension) View Subject | View Object

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MeSH
Arteries
MeSH
Sepsis
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Review

Evidence 4ddae796fa
JSON

Furthermore, a massive release of cytokines will shift the balance between pro- and anti-coagulatory factors in the blood, which will lead to increased coagulation of the blood (coagulopathy).

a(MESH:Cytokines) increases path(MESH:"Blood Coagulation Disorders") View Subject | View Object

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MeSH
Arteries
MeSH
Sepsis
Text Location
Review

Evidence 3b556f7e7b
JSON

Inhibition of the terminal complement cascade by eculizumab (inhibits the cleavage of C5 into C5a und C5b and thus the formation of the membrane attack complex 8, MAC C5b-C9) for the treatment of hemolytic paroxymal nocturnal hemoglobinuria (PNH) significantly prevented PNH-related symptoms in patients including abnormal thrombophilia, red blood cell destruction, and the extent of hemolysis [76].

a(MESH:eculizumab) decreases path(HP:"Paroxysmal nocturnal hemoglobinuria") View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

path(HP:"Hemolytic anemia") association path(HP:"Paroxysmal nocturnal hemoglobinuria") View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

path(HP:"Paroxysmal nocturnal hemoglobinuria") association path(MESH:Hemolysis) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

path(HP:"Paroxysmal nocturnal hemoglobinuria") association path(MESH:Thrombophilia) View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

path(HP:"Paroxysmal nocturnal hemoglobinuria") association path(HP:"Hemolytic anemia") View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

path(MESH:Hemolysis) association path(HP:"Paroxysmal nocturnal hemoglobinuria") View Subject | View Object

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

path(MESH:Thrombophilia) association path(HP:"Paroxysmal nocturnal hemoglobinuria") View Subject | View Object

Appears in Networks:
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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

Evidence 40134edddf
JSON

In a case report, Bull and Kuhn presented the pathogenesis of microangiopathic hemolytic anemia in a patient with an infiltrating adenocarcinoma [88]. In that patient, they found large numbers of micro-clots composed of fine fibrin strands in his vasculature.

bp(GO:"blood coagulation, fibrin clot formation") positiveCorrelation path(HP:"Microangiopathic hemolytic anemia") View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Adenocarcinoma
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path(HP:"Microangiopathic hemolytic anemia") positiveCorrelation bp(GO:"blood coagulation, fibrin clot formation") View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Adenocarcinoma
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Evidence 2c4ebb54ff
JSON

It is crucial, hence, to further investigate the mechanisms of sepsis-induced hemolysis with the aim of deriving possible therapeutic principles. Herein, we collected the most important previously known triggers of hemolysis during sepsis, which are (1) transfusion reactions and complement activation, (2) disseminated intravascular coagulation, (3) capillary stopped-flow, (4) restriction of glucose to red blood cells, (5) changes in red blood cell membrane properties, (6) hemolytic pathogens, and (7) red blood cell apoptosis.

bp(GO:"complement activation") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

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bp(MESH:"Glucose-Galactose Malabsorption") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

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path(MESH:"Disseminated Intravascular Coagulation") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

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path(MESH:"Transfusion Reaction") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

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path(MESH:Hemolysis) positiveCorrelation path(MESH:"Disseminated Intravascular Coagulation") View Subject | View Object

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path(MESH:Hemolysis) positiveCorrelation bp(GO:"complement activation") View Subject | View Object

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path(MESH:Hemolysis) positiveCorrelation path(MESH:"Transfusion Reaction") View Subject | View Object

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path(MESH:Hemolysis) positiveCorrelation bp(MESH:"Glucose-Galactose Malabsorption") View Subject | View Object

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Evidence 6bfb2a37cf
JSON

Thus, the complement system may be causally involved in the onset of hemolysis during sepsis [74] by directly damaging the red blood cells upon activation as a result of detecting pathogen structures [73].

bp(GO:"complement activation") increases path(MESH:Hemolysis) View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
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Evidence 62eac5ca3b
JSON

If glucose consumption further exceeds glucose production or uptake, finally hypoglycemia occurs [118].

bp(GO:"glucose catabolic process") increases path(MESH:Hypoglycemia) View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Disseminated Intravascular Coagulation
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Evidence 76cc983602
JSON

Extravascular hemolysis, however, results from Rh incompatibility of red blood cells [72] and is complement independent [71].

bp(HM:"Rh incompatibility") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

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Cell Ontology (CL)
erythrocyte
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Liver
MeSH
Sepsis
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path(MESH:Hemolysis) positiveCorrelation bp(HM:"Rh incompatibility") View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
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Evidence 14c87661cf
JSON

Nevertheless, the crosstalk between glucose and heme metabolism in sepsis is bidirectional since an excessive accumulation of cell-free heme following hemolysis influences the glucose metabolism by iron-driven oxidative inhibition of the glucose-6-phosphatase (a liver enzymes being important for endogenous glucose production via gluconeogenesis and glycogenolysis) [14].

bp(GO:"regulation of glucose-6-phosphatase activity") negativeCorrelation p(HGNC:HBB) View Subject | View Object

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Cell Ontology (CL)
erythrocyte
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Liver
MeSH
Sepsis
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p(HGNC:HBB) negativeCorrelation bp(GO:"regulation of glucose-6-phosphatase activity") View Subject | View Object

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Cell Ontology (CL)
erythrocyte
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Liver
MeSH
Sepsis
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Evidence b847f8edf3
JSON

Similar to HUS, during sepsis an activation not just of the complement system but also of the coagulation system has been described (essentially in consequence of the so-called pro-coagulant shift of the endothelial cells), which offers us the next possible cause of hemolysis during sepsis: destruction of the red blood cells in the fibrin mesh.

bp(MESH:"Blood Coagulation") increases path(MESH:Hemolysis) View Subject | View Object

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Cell Ontology (CL)
erythrocyte
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Liver
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Sepsis
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Evidence a09ee98ae9
JSON

Most hemolytic transfusion reactions^ can be attributed to ABO antibodies (ABO incompatibility of red blood cells) leading to intravascular hemolysis [69, 70] as a consequence of robust complement activation [71].

bp(MESH:"Blood Group Incompatibility") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

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Cell Ontology (CL)
hepatocyte
MeSH
Liver
MeSH
Sepsis
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Review

path(MESH:Hemolysis) positiveCorrelation bp(MESH:"Blood Group Incompatibility") View Subject | View Object

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Cell Ontology (CL)
hepatocyte
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Liver
MeSH
Sepsis
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Evidence 31f411f9ff
JSON

On the other hand, eryptosis is associated with anemia, microcirculatory derangement, and thrombosis [142, 144].

bp(MESH:Eryptosis) association path(MESH:Anemia) View Subject | View Object

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erythrocyte
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Liver
MeSH
Sepsis
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bp(MESH:Eryptosis) association path(MESH:Thrombosis) View Subject | View Object

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Cell Ontology (CL)
erythrocyte
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Liver
MeSH
Sepsis
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Review

path(MESH:Anemia) association bp(MESH:Eryptosis) View Subject | View Object

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Cell Ontology (CL)
erythrocyte
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Liver
MeSH
Sepsis
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path(MESH:Thrombosis) association bp(MESH:Eryptosis) View Subject | View Object

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Cell Ontology (CL)
erythrocyte
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Liver
MeSH
Sepsis
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Evidence eaa052f1e1
JSON

A higher glucose requirement is covered, then, by increased glycogenolysis and gluconeogenesis [37, 118].

bp(MESH:Gluconeogenesis) increases a(CHEBI:glucose) View Subject | View Object

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erythrocyte
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Liver
MeSH
Disseminated Intravascular Coagulation
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bp(MESH:Glycogenolysis) increases a(CHEBI:glucose) View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Disseminated Intravascular Coagulation
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Evidence 41d7e922ab
JSON

Finally, a bi-directional crosstalk between hemolysis and coagulation was postulated with induction of tissue factor by cell-free hemoglobin as potentially central mechanism for hemolysis to trigger coagulation [87].

p(HGNC:HBB) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
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path(MESH:Hemolysis) positiveCorrelation p(HGNC:HBB) View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
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Evidence bc13077452
JSON

One of the mechanisms by which cell-free hemoglobin exerts its detrimental effects is its ability to effectively scavenge nitric oxide (NO), which in turn leads to perfusion disorders and an increased arterial and pulmonary arterial pressure [39, 40].

p(HGNC:HBB) decreases a(CHEBI:"nitric oxide") View Subject | View Object

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Arteries
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Sepsis
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p(HGNC:HBB) increases path(MESH:Hypertension) View Subject | View Object

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Arteries
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Sepsis
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Evidence 18ba2569b9
JSON

Thus, the intravenous administration of hemoglobin in LPS-pretreated mice leads to a higher TNF- α concentration and an increased mortality; in turn, these effects could be inhibited by hemoglobin antibodies [33, 34].

p(HGNC:HBB) increases p(RGD:Tnf) View Subject | View Object

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Cell Ontology (CL)
hepatocyte
MeSH
Liver
MeSH
Sepsis
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Review

Evidence dacbca5a81
JSON

Heme released from cell-free hemoglobin on oxidation is bound by hemopexin and degraded by hepatocytes in the liver [12].

p(HGNC:HPX) decreases a(CHEBI:heme) View Subject | View Object

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Cell Ontology (CL)
hepatocyte
MeSH
Liver
MeSH
Sepsis
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Evidence 21f8e1484c
JSON

Vinchi and co-workers proved that the hemoglobin scavenger hemopexin prevents from hepatic microvascular stasis induced by intravascular hemolysis (using a mouse model of heme overloadin wild-typemicecomparedtohemopexin-nullmice) [116].

p(HGNC:HPX) decreases path(HM:"microvascular stasis") View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Disseminated Intravascular Coagulation
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Evidence ead063a153
JSON

Lipopolysaccharide (LPS)—the main constituent of the outer cell wall of Gram-negative bacteria—is known to bind to the pathogen recognition receptor TLR-4 and to activate the innate immune and hemostatic systems.

complex(a(CHEBI:lipopolysaccharide), p(HGNC:TLR4)) increases bp(MESH:"Immunity, Innate") View Subject | View Object

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erythrocyte
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Liver
MeSH
Sepsis
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complex(a(CHEBI:lipopolysaccharide), p(HGNC:TLR4)) increases bp(MESH:Hemostasis) View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
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Evidence e1e5e1a294
JSON

Once cell-free hemoglobin was bound by its scavenger haptoglobin, the resulting haptoglobin–hemoglobin complex will bind to CD163 on the surface of macrophages/monocytes to initiate endocytosis and degradation of the complex [12, 39].

complex(a(MESH:"haptoglobin-hemoglobin complex"), p(HGNC:CD163)) increases bp(MESH:Endocytosis) View Subject | View Object

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Cell Ontology (CL)
macrophage
MeSH
Arteries
MeSH
Sepsis
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Review

Evidence d1de605828
JSON

Normally, cellfree hemoglobin will dimerize and rapidly be bound by its hemoglobin scavengers haptoglobin and hemopexin [12].

p(HGNC:HP) decreases p(HGNC:HBB) View Subject | View Object

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Arteries
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Sepsis
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Evidence 319c883ae0
JSON

The same applies to hemolysin. For one thing, the pore-forming toxin hemolysin is one the pathogens’ tools of causing hemolysis or releasing hemoglobin and poorly available iron [139]; then again it trigger eryptosis, one mechanism of protecting against hemolysis [142].

p(PFAM:Leukocidin) increases bp(MESH:Eryptosis) View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
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Review

p(PFAM:Leukocidin) increases path(MESH:Hemolysis) View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
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Review

p(PFAM:Leukocidin) increases p(HGNC:HBB) View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
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Review

Evidence 6c73761a72
JSON

From hemolytic uremic syndrome (HUS), we know that damage to the endothelium (endothelial lesions) might be the primary cause of hemolysis.

path(HM:"endothelial lesions") increases path(MESH:Hemolysis) View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Atypical Hemolytic Uremic Syndrome
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Evidence 4f7bccfbef
JSON

During HUS, endothelial lesions cause a complement dependent activation of immune response and local thrombus formation—attachment of fibrin and platelets to the endothelial lesions and consequently disseminated intravascular coagulation (DIC)—and further mechanical destruction of the red blood cells in the fibrin mesh resulting in hemolysis [82].

path(HM:"endothelial lesions") increases path(MESH:Hemolysis) View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Atypical Hemolytic Uremic Syndrome
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path(HM:"endothelial lesions") increases path(MESH:Thrombosis) View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Atypical Hemolytic Uremic Syndrome
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Review

path(HM:"endothelial lesions") increases path(MESH:"Disseminated Intravascular Coagulation") View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Atypical Hemolytic Uremic Syndrome
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Evidence 20ae626383
JSON

There are various studies that show a relationship between microvascular stasis and intravascular hemolysis. Already in 1940, Mumme described that renal stasis causes hemolysis [108].

path(HM:"renal stasis") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
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path(MESH:Hemolysis) positiveCorrelation path(HM:"renal stasis") View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
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Evidence 1c90462279
JSON

On the other hand, impaired microcirculation in the tissue usually causes local ischemia (circulatory disorders and lack of oxygen in the tissue) and often results in multiple organ failure [31].

path(HP:"Abnormality of blood circulation") increases path(MESH:Ischemia) View Subject | View Object

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Sepsis
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path(MESH:Ischemia) increases path(MESH:"Multiple Organ Failure") View Subject | View Object

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Arteries
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Evidence 00548f72df
JSON

They concluded that intravascular coagulation must be the most likely cause of this microangiopathic hemolytic anemia.

path(HP:"Microangiopathic hemolytic anemia") positiveCorrelation path(MESH:"Disseminated Intravascular Coagulation") View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Adenocarcinoma
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path(MESH:"Disseminated Intravascular Coagulation") positiveCorrelation path(HP:"Microangiopathic hemolytic anemia") View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Adenocarcinoma
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Evidence e13292e1eb
JSON

A severe sepsis further was defined as sepsis with organ dysfunction and a septic shock as severe sepsis with cardiovascular collapse that does not respond to fluid intake [23].

path(MESH:"Cardiovascular Infections") positiveCorrelation path(MESH:"Shock, Septic") View Subject | View Object

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path(MESH:"Shock, Septic") positiveCorrelation path(MESH:"Cardiovascular Infections") View Subject | View Object

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Evidence c8e3b75b7b
JSON

DIC is characterized by a systemic intravascular coagulation, formation of microvascular thrombi, insufficiently compensated consumption of platelets and coagulation factors, and eventually bleeding tendency [84].

path(MESH:"Disseminated Intravascular Coagulation") positiveCorrelation path(MESH:Thrombosis) View Subject | View Object

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erythrocyte
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Microvessels
MeSH
Sepsis
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path(MESH:"Disseminated Intravascular Coagulation") positiveCorrelation path(MESH:Thrombocytopenia) View Subject | View Object

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erythrocyte
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path(MESH:Thrombocytopenia) positiveCorrelation path(MESH:"Disseminated Intravascular Coagulation") View Subject | View Object

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erythrocyte
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Microvessels
MeSH
Sepsis
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path(MESH:Thrombosis) positiveCorrelation path(MESH:"Disseminated Intravascular Coagulation") View Subject | View Object

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erythrocyte
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Microvessels
MeSH
Sepsis
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Evidence 0a331a0875
JSON

Sepsis/systemic inflammation is frequently associated with disseminated intravascular coagulation (DIC) being a predictor of mortality in septic patients [84, 85].

path(MESH:"Disseminated Intravascular Coagulation") association path(MESH:Inflammation) View Subject | View Object

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erythrocyte
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Liver
MeSH
Sepsis
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path(MESH:Inflammation) association path(MESH:"Disseminated Intravascular Coagulation") View Subject | View Object

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Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
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Evidence c79e5e7fed
JSON

Thus, hemolysis can act as a kind of amplifier of the complex response to an infection or injury [8, 15] and worsen the outcome from animals and patients with systemic inflammation, sepsis, or trauma [1–4, 10].

path(MESH:Hemolysis) positiveCorrelation path(MESH:Sepsis) View Subject | View Object

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path(MESH:"Shock, Traumatic") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

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path(MESH:Hemolysis) positiveCorrelation path(MESH:Inflammation) View Subject | View Object

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path(MESH:Hemolysis) positiveCorrelation path(MESH:"Shock, Traumatic") View Subject | View Object

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path(MESH:Inflammation) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

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path(MESH:Sepsis) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

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Evidence 720e60e0c2
JSON

Crucial for a sepsis, thus, was the presence of at least two of four criteria of a systemic inflammatory response syndrome (SIRS), which includes (1) fever (≥ 38.0 °C) or hypothermia (≤ 36.0 °C), (2) tachycardia (heart rate ≥ 90/min), (3) tachypnea (frequency ≥ 20/min) or hyperventilation, and (4) leukocytosis (white blood cells ≥ 12,000/mm3) or leukopenia (white blood cells ≤ 4000/mm3).

path(MESH:"Systemic Inflammatory Response Syndrome") positiveCorrelation path(MESH:Hypothermia) View Subject | View Object

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path(MESH:"Systemic Inflammatory Response Syndrome") positiveCorrelation path(MESH:Tachycardia) View Subject | View Object

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path(MESH:"Systemic Inflammatory Response Syndrome") positiveCorrelation path(MESH:Hyperventilation) View Subject | View Object

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Review

path(MESH:"Systemic Inflammatory Response Syndrome") positiveCorrelation path(MESH:Leukocytosis) View Subject | View Object

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path(MESH:"Systemic Inflammatory Response Syndrome") positiveCorrelation path(MESH:Leukopenia) View Subject | View Object

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path(MESH:Hyperventilation) positiveCorrelation path(MESH:"Systemic Inflammatory Response Syndrome") View Subject | View Object

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path(MESH:Hyperventilation) positiveCorrelation path(MESH:Sepsis) View Subject | View Object

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path(MESH:Hypothermia) positiveCorrelation path(MESH:"Systemic Inflammatory Response Syndrome") View Subject | View Object

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path(MESH:Hypothermia) positiveCorrelation path(MESH:Sepsis) View Subject | View Object

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path(MESH:Leukocytosis) positiveCorrelation path(MESH:"Systemic Inflammatory Response Syndrome") View Subject | View Object

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path(MESH:Leukocytosis) positiveCorrelation path(MESH:Sepsis) View Subject | View Object

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Review

path(MESH:Leukopenia) positiveCorrelation path(MESH:"Systemic Inflammatory Response Syndrome") View Subject | View Object

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Review

path(MESH:Leukopenia) positiveCorrelation path(MESH:Sepsis) View Subject | View Object

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path(MESH:Sepsis) positiveCorrelation path(MESH:Hypothermia) View Subject | View Object

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path(MESH:Sepsis) positiveCorrelation path(MESH:Tachycardia) View Subject | View Object

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Review

path(MESH:Sepsis) positiveCorrelation path(MESH:Hyperventilation) View Subject | View Object

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Review

path(MESH:Sepsis) positiveCorrelation path(MESH:Leukocytosis) View Subject | View Object

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path(MESH:Sepsis) positiveCorrelation path(MESH:Leukopenia) View Subject | View Object

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path(MESH:Tachycardia) positiveCorrelation path(MESH:"Systemic Inflammatory Response Syndrome") View Subject | View Object

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path(MESH:Tachycardia) positiveCorrelation path(MESH:Sepsis) View Subject | View Object

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Evidence 40ffcebd23
JSON

Both clinical [1–4] and experimental [5–8] studies have shown that sepsis and systemic inflammation lead to a massive release of hemoglobin from red blood cells (hemolysis) being accompanied with an increased risk of death [1–4, 8, 9].

path(MESH:Hemolysis) positiveCorrelation path(MESH:Sepsis) View Subject | View Object

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path(MESH:Sepsis) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

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Evidence de0c56d19c
JSON

Furthermore, fibrinolysis (dissolution of a blood clot) is also regularly inhibited in the early stages of sepsis [86].

path(MESH:Sepsis) decreases path(MESH:Fibrinolysis) View Subject | View Object

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Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Sepsis
Text Location
Review

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.