Programmed cell death in cardiac myocytes: strategies to maximize post-ischemic salvage.
The most common cause of systolic dysfunction in the United States is prior ischemic injury. As the basic functional unit of the myocardium, the cardiac myocyte is the ultimate target of both the pathogenesis and possible therapies in this paradigm. Maintaining adequate numbers of these terminally differentiated units in the myocardium has been the focus of all therapies in ischemic syndromes, including reperfusion strategies. Programmed cell death, in the forms of apoptosis, necrosis and possibly, autophagic cell death are the final arbiters of myocyte numbers following myocardial infarction. This review will focus on the evidence for cell death in the development of heart failure following myocardial infarction, a brief review of the relevant pathways and the targets for development of future therapies.
Mani
Kartik
K
Cardiovascular Research Center, Albert Einstein College of Medicine, Golding G-01, Morris Park Av., Bronx, NY 10461, USA. kmani@montefiore.org
D000818:Animals; D001343:Autophagy; D006333:Heart Failure / Q000209:etiology / Q000473:pathology / Q000517:prevention & control; D006801:Humans; D009203:Myocardial Infarction / Q000150:complications / Q000473:pathology / Q000628:therapy*; D015425:Myocardial Reperfusion / Q000379:methods*; D032383:Myocytes, Cardiac / Q000473:pathology*