a(MESH:"Erythrocytes, Abnormal")
Phosphatidylserine externalization and shedding are mediated by increased cellular Ca-flux and play an important role in natural RBC senescence [44]. PubMed:28458720
Under conditions of apoptosis or RBC damage, such as high shear rates, inflammation, or oxidative stress, RBCs can lose membrane asymmetry and expose phosphatidylserine [43]. PubMed:28458720
Under conditions of apoptosis or RBC damage, such as high shear rates, inflammation, or oxidative stress, RBCs can lose membrane asymmetry and expose phosphatidylserine [43]. PubMed:28458720
In contrast, RBCs impair contraction and reduce stiffness, while increasing the overall contractile stress generated by the platelet-fibrin meshwork [75, 76, 85]. PubMed:28458720
Under conditions of apoptosis or RBC damage, such as high shear rates, inflammation, or oxidative stress, RBCs can lose membrane asymmetry and expose phosphatidylserine [43]. PubMed:28458720
Under conditions of apoptosis or RBC damage, such as high shear rates, inflammation, or oxidative stress, RBCs can lose membrane asymmetry and expose phosphatidylserine [43]. PubMed:28458720
Damaged RBCs also release arginase that cleaves L-arginine, a substrate for NO production [29]. PubMed:28458720
When RBCs are damaged by high shear in continuous flow ventricular assist devices, free hemoglobin induces platelet aggregation, contributing to high risk of thrombotic complications [33]. PubMed:28458720
Under conditions of apoptosis or RBC damage, such as high shear rates, inflammation, or oxidative stress, RBCs can lose membrane asymmetry and expose phosphatidylserine [43]. PubMed:28458720
Under conditions of apoptosis or RBC damage, such as high shear rates, inflammation, or oxidative stress, RBCs can lose membrane asymmetry and expose phosphatidylserine [43]. PubMed:28458720
Under conditions of apoptosis or RBC damage, such as high shear rates, inflammation, or oxidative stress, RBCs can lose membrane asymmetry and expose phosphatidylserine [43]. PubMed:28458720
Under conditions of apoptosis or RBC damage, such as high shear rates, inflammation, or oxidative stress, RBCs can lose membrane asymmetry and expose phosphatidylserine [43]. PubMed:28458720
Phosphatidylserine externalization and shedding are mediated by increased cellular Ca-flux and play an important role in natural RBC senescence [44]. PubMed:28458720
As a generality, incorporation of RBCs increases the lytic resistance and decreases the permeability of fibrin in a dose-dependent manner [79, 80]. PubMed:28458720
In contrast, RBCs impair contraction and reduce stiffness, while increasing the overall contractile stress generated by the platelet-fibrin meshwork [75, 76, 85]. PubMed:28458720
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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.