Affiliation:
1. From the Molecular Cardiology Unit (W.R.M., M.D.S.), the Departments of Medicine (W.R.M.), Cell Biology (M.D.S.), and Molecular Physiology & Biophysics (M.D.S.), and Houston Veterans Affairs Medical Center (W.R.M.), Baylor College of Medicine, Houston, Tex.
Abstract
Abstract
Programmed cell death (apoptosis) is recognized, increasingly, as a contributing cause of cardiac myocyte loss with ischemia/reperfusion injury, myocardial infarction, and long-standing heart failure. Although the exact mechanisms initiating apoptosis in these in vivo settings remain unproven, insights into the molecular circuitry controlling apoptosis more widely suggest the potential to protect mammalian ventricular muscle from apoptosis through one or more of these pathways, by pharmacological means or, conceivably, gene transfer.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Subject
Cardiology and Cardiovascular Medicine,Physiology
Cited by
307 articles.
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