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MG53 Constitutes a Primary Determinant of Cardiac Ischemic Preconditioning
Author(s) -
Chunmei Cao,
Yan Zhang,
Noah Weisleder,
Christopher Ferrante,
Xianhua Wang,
Fengxiang Lv,
Yi Zhang,
Ruisheng Song,
Moonsun Hwang,
Jin Li,
Jiaojiao Guo,
Wei Peng,
Geng Li,
Miyuki Nishi,
Hiroshi Takeshima,
Jianjie Ma,
RuiPing Xiao
Publication year - 2010
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.110.954628
Subject(s) - medicine , ischemic preconditioning , ischemia , reperfusion injury , cardioprotection , protein kinase b , downregulation and upregulation , pi3k/akt/mtor pathway , hypoxia (environmental) , cardiology , signal transduction , microbiology and biotechnology , biology , biochemistry , chemistry , organic chemistry , oxygen , gene
Ischemic heart disease is the greatest cause of death in Western countries. The deleterious effects of cardiac ischemia are ameliorated by ischemic preconditioning (IPC), in which transient ischemia protects against subsequent severe ischemia/reperfusion injury. IPC activates multiple signaling pathways, including the reperfusion injury salvage kinase pathway (mainly PI3K-Akt-glycogen synthase kinase-3beta [GSK3beta] and ERK1/2) and the survivor activating factor enhancement pathway involving activation of the JAK-STAT3 axis. Nevertheless, the fundamental mechanism underlying IPC is poorly understood.

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