Mechanism of Hepatic Ischemia/Reperfusion Injury and Protection Against Reperfusion Injury

Authors
K.J. Kang
Department
Dept. of Surgery (외과학)
Issue Date
2002
Citation
Transplantation Proceedings, Vol.34(7) : 2659-2661, 2002
ISSN
0041-1345
Abstract
THE ISCHEMIA/REPERFUSION injury remains a problem after liver surgery or liver transplantation. Preservation injury is a major cause of primary nonfunction following liver transplantation. Sinusoidal endothelial cell (SEC) apoptosis is an outcome of cold ischemia/reperfusion injury. Investigators demonstrated a selective induction of apoptosis in sinusoidal and vascular endothelial cells within the liver following cold ischemia/warm reperfusion injury. Recent data also have indicated that platelet and leukocyte adhesion to the sinusoids mediate reperfusion injury by causing endothelial cell apoptosis. Ischemic precondition- ing, namely, a short period of ischemia prior to a major ischemic insult, is highly protective to downregulate the caspase pathway and inhibit apoptotic cell death.¹,² Future research on ischemic livers should focus on mechanisms and mediators involved in apoptotic cell death, which may lead to innovative protective strategies and preservation solutions with important clinical implications.
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/34755
Appears in Collections:
1. Journal Papers (연구논문) > 1. School of Medicine (의과대학) > Dept. of Surgery (외과학)
Keimyung Author(s)
강구정
Full Text
https://www.sciencedirect.com/science/article/pii/S0041134502034656?via%3Dihub
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