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PubMed: 26475040

Title
Different target specificities of haptoglobin and hemopexin define a sequential protection system against vascular hemoglobin toxicity.
Journal
Free radical biology & medicine
Volume
89
Issue
None
Pages
931-43
Date
2015-12-01
Authors
Buehler PW | Deuel JW | Puglia M | Schaer CA | Schaer DJ | Vallelian F

Evidence fd8550a4b8
JSON

Oxidized LP(ox- LP) then induces toxic effects in endothelial cells [6].

a(CHEBI:"oxidised LDL") increases path(HM:"Endothelial dysfunction") View Subject | View Object

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MeSH
Anemia, Sickle Cell
Text Location
Abstract

Evidence dd772652f6
JSON

Many studies have explored basic mechanisms of Hb or heme triggered endothelial damage and have suggested that oxidative reactions of Hb generate multiple toxic species such as free heme that is released from ferric Hb, iron, free radicals, and globin aggregation products [15],[16],[17],[18],[19],[20],[21],[22],[23],[24],[25].

a(CHEBI:heme) increases path(HM:"Endothelial dysfunction") View Subject | View Object

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MeSH
Anemia, Sickle Cell
Text Location
Abstract

p(HGNC:HBB) increases path(HM:"Endothelial dysfunction") View Subject | View Object

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MeSH
Anemia, Sickle Cell
Text Location
Abstract

Evidence d3a10d4ac0
JSON

Free hemoglobin (Hb) triggered vascular damage occurs in many hemolytic diseases, such as sickle cell disease, with an unmet need for specific therapeutic interventions.

p(HGNC:HBB) increases path(MESH:"Vascular System Injuries") View Subject | View Object

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MeSH
Anemia, Sickle Cell
Text Location
Abstract

Evidence 733d028294
JSON

Depending on the scale, rate, and site of hemolysis, the primary adverse effects triggered by free Hb are vascular dysfunction, oxidative tissue damage, and altered inflammatory response [1],

p(HGNC:HBB) increases path(MESH:"Vascular System Injuries") View Subject | View Object

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MeSH
Anemia, Sickle Cell
Text Location
Abstract

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

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MeSH
Anemia, Sickle Cell
Text Location
Abstract

p(HGNC:HBB) increases bp(MESH:"Oxidative Stress") View Subject | View Object

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MeSH
Anemia, Sickle Cell
Text Location
Abstract

Evidence bf0ba8844c
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Based on clinical observations the Hb and heme scavenger proteins haptoglobin (Hp) and hemopexin (Hx) have been characterized as a sequential defense system with Hp as the primary protector and Hx as a backup when all Hp is depleted during more severe intravascular hemolysis.

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

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MeSH
Anemia, Sickle Cell
Text Location
Abstract

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

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MeSH
Anemia, Sickle Cell
Text Location
Abstract

Evidence b9aa336495
JSON

However, in patients with hemolysis Hp depletes early in the course of the disease while levels of Hx remain within the physiologic range for prolonged periods of sustained hemolytic disease [12].

p(HGNC:HP) negativeCorrelation path(MESH:Hemolysis) View Subject | View Object

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MeSH
Anemia, Sickle Cell
Text Location
Abstract

path(MESH:Hemolysis) negativeCorrelation p(HGNC:HP) View Subject | View Object

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MeSH
Anemia, Sickle Cell
Text Location
Abstract

Evidence 073f3a15c7
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Systemic hemolysis occurs during certain genetic and acquired anemia, such as in sickle cell disease and malaria.

path(MESH:"Anemia, Sickle Cell") increases path(MESH:Hemolysis) View Subject | View Object

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MeSH
Anemia, Sickle Cell
Text Location
Abstract

path(MESH:Malaria) increases path(MESH:Hemolysis) View Subject | View Object

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MeSH
Anemia, Sickle Cell
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Abstract

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