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

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Author(s)
K.J. Kang
Publication Year
2002
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.
Department
Dept. of Surgery (외과학)
Publisher
School of Medicine
Citation
Transplantation Proceedings, Vol.34(7) : 2659-2661, 2002
Type
Article
ISSN
0041-1345
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/34755
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