Review |
From the Department of Medicine (M.T.C.), Johns Hopkins University School of Medicine, Baltimore Md; and the Departments of Medicine and Cell Biology, Cardiovascular Research Center (K.M., Y.-J.N., R.N.K.), and Cancer Center (R.N.K.), Albert Einstein College of Medicine, Bronx, NY.
Correspondence to Michael T. Crow, Department of Medicine, Johns Hopkins University School of Medicine, 5501 Hopkins Bayview Circle, Rm 5A.58, Baltimore, MD 21224; E-mail mcrow1{at}jhmi.edu; and to Richard N. Kitsis, Cardiovascular Research Center, Albert Einstein College of Medicine, 1300 Morris Park Ave, Bronx, NY 10461. E-mail kitsis{at}aecom.yu.edu
This Review is part of a thematic series on Mitochondrial Dysfunction in Ischemia, which includes the following articles:
Role of the Mitochondrial Permeability Transition in Myocardial Disease
Primary and Secondary Signaling Pathways in Early Preconditioning That Converge on the Mitochondria to Produce Cardioprotection
Evidence for Mitochondrial K+ Channels and their Role in Cardioprotection
The Mitochondrial Death Pathway and Cardiac Myocyte Apoptosis
Elizabeth Murphy, Guest Editor; Roberto Bolli, Editor
Apoptosis has been causally linked to the pathogenesis of myocardial infarction and heart failure in rodent models. This death process is mediated by two central pathways, an extrinsic pathway involving cell surface receptors and an intrinsic pathway using mitochondria and the endoplasmic reticulum. Each of these pathways has been implicated in myocardial pathology. In this review, we summarize recent advances in the understanding of the intrinsic pathway and how it relates to cardiac myocyte death and heart disease.
Key Words: apoptosis necrosis cell death mitochondria Bcl-2 caspase death-inducing signaling complex apoptosome ischemia heart failure
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