Cardioprotection against reperfusion injury: updated mechanisms and strategies / 生理学报
Acta Physiologica Sinica
; (6): 553-561, 2007.
Article
in English
| WPRIM (Western Pacific)
| ID: wpr-258622
Responsible library:
WPRO
ABSTRACT
Early restoration of blood flow to the ischemic myocardium not only saves myocardium but also induces reperfusion injury. While no specific therapy to reduce reperfusion injury has yet been established, recent laboratory studies have shown that G protein-coupled receptor (GPCR) agonists, insulin, and postconditioning can effectively prevent reperfusion injury in various experimental settings and animal species. The potential mechanisms underlying the cardioprotection initiated by these interventions may include activation of the reperfusion injury salvage kinase (RISK) pathway, inactivation of glycogen synthase kinase 3beta (GSK-3beta), and modulation of mitochondrial permeability transition pore (mPTP) opening. These encouraging laboratory findings may help us develop successful clinical strategies to salvage reperfused myocardium in patients with acute myocardial infarction.
Full text:
Available
Database:
WPRIM (Western Pacific)
Main subject:
Physiology
/
Myocardial Reperfusion Injury
/
Glycogen Synthase Kinase 3
/
Mitochondrial Membrane Transport Proteins
/
Metabolism
/
Myocardial Infarction
/
Myocardium
Limits:
Humans
Language:
English
Journal:
Acta Physiologica Sinica
Year:
2007
Document type:
Article