Mitochondrial Death Channels

Figure 1. A 53-year-old patient experiencing sporadic discomfort undergoes a coronary angiogram. The results are ominous. Severe stenosis (narrowing) is visible in the pinched regions (top middle), indicating the buildup of fatty deposits within the artery. If a wandering clot blocks the pinhole opening of a nearly clogged vessel, a heart attack ensues. With bloodflow blocked, cardiac cells downstream are starved for oxygen, leading to drastic metabolic changes as the cells struggle to survive. The most important changes affect mitochondria, the powerhouses of cell metabolism. The inset shows mitochondria (orange) arrayed among cardiac muscle fibrils (blue), where they are positioned to supply a steady stream of ATP to contracting muscle. Under oxidative stress, the mitochondria can also release potent effectors that lead directly to apoptosis—cell suicide. The trigger for the opening of the so-called mitochondrial death channels is, ironically, the return of oxygen to starved tissue during reperfusion. Learning to control the activities of the death channels could vastly improve the outlook for heart attack victims.

Top image by Zephyr/Photo Researchers, Inc.; bottom image by Steve Gschmeissner/Photo Researchers, Inc.

From American Scientist:

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.

Coronary artery disease is the leading cause of morbidity and mortality in North America and Europe. 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). Chronic stable angina (chest pain) is the initial manifestation of coronary artery disease in approximately half of all presenting patients, and about 16.5 million Americans (more than 5 percent) currently have stable angina.

Read more ....