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Involvement of Rho-Kinase in Cold Ischemia-Reperfusion Injury after Liver Transplantation in Rats
Author(s) -
Satoko Shiotani,
Mitsuo Shimada,
Taketoshi Suehiro,
Yuji Soejima,
Tomoharu Yosizumi,
Hiroaki Shimokawa,
Yoshihiko Maehara
Publication year - 2004
Publication title -
transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.45
H-Index - 204
eISSN - 1534-6080
pISSN - 0041-1337
DOI - 10.1097/01.tp.0000128618.41619.e7
Subject(s) - fasudil , reperfusion injury , medicine , rho kinase inhibitor , pharmacology , rho associated protein kinase , transplantation , reactive oxygen species , ischemia , necrosis , liver transplantation , tumor necrosis factor alpha , apoptosis , oxidative stress , in vivo , proinflammatory cytokine , kinase , immunology , chemistry , pathology , inflammation , biology , biochemistry , microbiology and biotechnology
Reperfusion of ischemic tissues is known to cause the generation of reactive oxygen species (ROS) with resultant tissue damage. However, the sources of ROS in reperfused tissues are not fully characterized. We hypothesized that the small GTPase Rho and its target effector Rho-kinase/ROK/ROCK are involved in the oxidative burst in reperfused tissue with resultant reperfusion injury.

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