path(HM:"endothelial lesions")
Endothelial injury may also be related to Free hemoglobin and its breakdown oxidative product heme, and MPs, which mediates direct proinflammatory, proliferative, and pro-oxidant effects on endothelial cells [22–24] both in PNH and congenital CD59 deficiency, but may be more pronounced in congenital CD59 deficiency and perhaps even more in the brain due to loss of CD59 in the endothelium of these patients. PubMed:29929138
Endothelial injury may also be related to Free hemoglobin and its breakdown oxidative product heme, and MPs, which mediates direct proinflammatory, proliferative, and pro-oxidant effects on endothelial cells [22–24] both in PNH and congenital CD59 deficiency, but may be more pronounced in congenital CD59 deficiency and perhaps even more in the brain due to loss of CD59 in the endothelium of these patients. PubMed:29929138
Endothelial injury may also be related to Free hemoglobin and its breakdown oxidative product heme, and MPs, which mediates direct proinflammatory, proliferative, and pro-oxidant effects on endothelial cells [22–24] both in PNH and congenital CD59 deficiency, but may be more pronounced in congenital CD59 deficiency and perhaps even more in the brain due to loss of CD59 in the endothelium of these patients. PubMed:29929138
Injured endothelium may provide tissue factors and additional prothrombotic factors [21] that are not a prothrombotic mechanism in PNH. PubMed:29929138
Injured endothelium may provide tissue factors and additional prothrombotic factors [21] that are not a prothrombotic mechanism in PNH. PubMed:29929138
Endothelial injury may also be related to Free hemoglobin and its breakdown oxidative product heme, and MPs, which mediates direct proinflammatory, proliferative, and pro-oxidant effects on endothelial cells [22–24] both in PNH and congenital CD59 deficiency, but may be more pronounced in congenital CD59 deficiency and perhaps even more in the brain due to loss of CD59 in the endothelium of these patients. PubMed:29929138
Endothelial injury may also be related to Free hemoglobin and its breakdown oxidative product heme, and MPs, which mediates direct proinflammatory, proliferative, and pro-oxidant effects on endothelial cells [22–24] both in PNH and congenital CD59 deficiency, but may be more pronounced in congenital CD59 deficiency and perhaps even more in the brain due to loss of CD59 in the endothelium of these patients. PubMed:29929138
Endothelial injury may also be related to Free hemoglobin and its breakdown oxidative product heme, and MPs, which mediates direct proinflammatory, proliferative, and pro-oxidant effects on endothelial cells [22–24] both in PNH and congenital CD59 deficiency, but may be more pronounced in congenital CD59 deficiency and perhaps even more in the brain due to loss of CD59 in the endothelium of these patients. PubMed:29929138
From hemolytic uremic syndrome (HUS), we know that damage to the endothelium (endothelial lesions) might be the primary cause of hemolysis. PubMed:29956069
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]. PubMed:29956069
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]. PubMed:29956069
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]. PubMed:29956069
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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.