FEATURE ARTICLE
Mitochondrial Death Channels
In heart attacks, cells die if they aren’t perfused with fresh oxygen—and kill themselves if they are. Understanding cell suicide may greatly improve outcomes
Keith A. Webster
More than 12 million people in the United States have coronary artery disease, and more than 7 million have had a myocardial infarction (heart attack). Surgical interventions to prevent or treat acute myocardial infarction are increasing: More than 1 million coronary angioplasty and coronary artery bypass procedures were performed in 2000 in the U.S. A major goal of clinical research is to establish treatment criteria that will limit the damage from myocardial infarction. Mitochondria, the powerhouses of the cell, are the central players in defining the outcome of heart attacks. Mitochondria contain cellular poisons that are normally sequestered but that enforce cell suicide when unleashed. These suicide regulators emerge from mitochondria through so-called death channels. Understanding how death channels work may hold the key to new treatments that could dramatically reduce myocardial injury for heart-attack victims.
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