Abstract

Many of the adverse sequelae of acute myocardial ischemia result from the degradation of sarcolemmal phospholipid constituents mediated by the activation of intracellular phospholipases. The consequent deleterious changes in sarcolemmal membrane properties precipitate ischemic membrane dysfunction resulting in electrophysiologic alterations and myocytic cell death. In myocardium, the overwhelming majority of phospholipase activity is catalyzed by a novel class of calcium-independent plasmalogen-selective phospholipases A2 that is rapidly and reversibly activated within minutes of myocardial ischemia. Elucidation of the molecular mechanisms underlying the regulation of these phospholipases A2 will define novel therapeutic targets that can potentially be pharmacologically manipulated to attenuate the deleterious effects of ischemia and reperfusion on myocardial function.

Original languageEnglish
Pages (from-to)115-121
Number of pages7
JournalTrends in Cardiovascular Medicine
Volume2
Issue number3
DOIs
StatePublished - 1992

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