Insulin: An overall cardiovascular protector?

Published on Dec 15, 2005in Cardiovascular Research7.014
· DOI :10.1016/j.cardiores.2005.11.017
Yaser Abdallah22
Estimated H-index: 22
(University of Giessen),
Claudia Schäfer18
Estimated H-index: 18
(University of Giessen)
See article by Ma et al. [4] (pages 57–65) in this issue. Protection of myocardium against lethal reperfusion injury is one of the major challenges of clinical cardiology today. Many interventions during reperfusion that may influence infarct size or improve cardiac function have been studied experimentally, but none of these has yet found its way into clinical practice. One of the oldest and most discussed interventions to modify reperfusion conditions is the use of glucose–insulin–potassium (GIK) [1], which was reported to reduce the relative in-hospital mortality risk in patients with acute myocardial infarction [2]. Administration of insulin in vivo was shown to reduce reperfusion-induced cell death through a signalling pathway comprising PI 3-kinase (PI3K)/Akt and nitric oxide synthase (eNOS) [3]. The experimental study by Ma et al. [4] in this issue of Cardiovascular Research provides an interesting contribution, focusing for the first time on the role of GIK and particularly its leading actor, insulin, for prevention of reperfusion-induced vascular injury in the heart. Various mechanisms contributing to cardiac reperfusion injury have been described, but protective strategies share ultimately the same goal, i.e., prevention of cell death and improvement … *Corresponding author. Tel.: +49 641 99 47 221; fax: +49 641 99 47 219. Email address: yaser.abdallah{at}
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