Cardioprotection requires flipping the 'posttranslational modification' switch.

Autor: Porter K; Program in Nutrition and Exercise Physiology, Washington State University, Spokane, WA, USA., Medford HM, McIntosh CM, Marsh SA
Jazyk: angličtina
Zdroj: Life sciences [Life Sci] 2012 Jan 16; Vol. 90 (3-4), pp. 89-98. Date of Electronic Publication: 2011 Dec 03.
DOI: 10.1016/j.lfs.2011.10.026
Abstrakt: Minimizing damage during reperfusion of the heart following an ischemic event is an important part of the recovery process, as is preventing future recurrences; however, restoring blood perfusion to the heart following ischemia can lead to apoptosis, necrosis, and finally, diminished cardiac function. Exercise reduces risk of heart disease and has been shown to improve the recovery of the heart following ischemia and reperfusion. Brief intermittent ischemic events administered prior to or following a myocardial infarction have also been demonstrated to reduce the infarct size and improve cardiac function, thereby providing cardioprotection. Many signaling transduction pathways are known to regulate cardioprotection, including but not limited to calcium regulation, antioxidant scavenging, and kinase activation. Although posttranslational modifications (PTM) such as phosphorylation, O-GlcNAcylation, methylation, and acetylation are essential regulators of these pathways, their contributions are often overlooked in the literature. This review will examine how PTMS are important regulators of cardioprotection and demonstrate why they should be targeted when developing future therapies for the minimization of damage caused by cardiac ischemia and reperfusion.
(Copyright © 2011 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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