Mitochondrial permeability transition in cardiac cell injury and death.

Cardiovasc Drugs Ther

Department of Medicine, David Geffen School of Medicine at the University of California, Los Angeles, CA 90095-1679, USA.

Published: December 2006

AI Article Synopsis

  • Mitochondria play a crucial role in determining how cells respond to stress, particularly during ischemia/reperfusion (I/R) injuries, like those from heart attacks and strokes.
  • Mitochondrial permeability transition (MPT) refers to changes in the mitochondrial membrane that can lead to different cell fates based on its severity—minimal MPT allows recovery, moderate leads to programmed cell death, and severe results in cell necrosis from energy failure.
  • The text reviews the impact of MPT in diseases, explores the signaling pathways that control it, and discusses the future challenges in researching MPT.

Article Abstract

Mitochondria can serve as the arbiter of cell fate in response to stress. Mitochondrial permeability transition (MPT) is characterized by permeabilization of an otherwise relatively impermeable mitochondrial inner membrane and appears to have a major role in ischemia/reperfusion (I/R) injury in myocardial infarction and stroke. After I/R, the fate of the cell is determined by the extent of MPT. If minimal, the cell may recover; if moderate, the cell may undergo programmed cell death; if severe, the cell may die from necrosis due to inadequate energy production. After reviewing the role of MPT in disease, we examine the signaling and metabolic networks that regulate MPT. We then conclude with some of the challenges in future MPT research.

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Source
http://dx.doi.org/10.1007/s10557-006-0642-0DOI Listing

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