Mitochondrial permeability transition: A common pathway to necrosis and apoptosis

Jae Sung Kim, Lihua He, John J. Lemasters

Research output: Contribution to journalArticle

570 Scopus citations

Abstract

Opening of high conductance permeability transition pores in mitochondria initiates onset of the mitochondrial permeability transition (MPT). The MPT is a causative event, leading to necrosis and apoptosis in hepatocytes after oxidative stress, Ca2+ toxicity, and ischemia/reperfusion. Cyclosporin A blocks opening of permeability transition pores and protects cell death after these stresses. In contrast to necrotic cell death which is a consequence of ATP depletion, ATP is required for the development of apoptosis. Reperfusion and the return of normal pH after ischemia initiate the MPT, but the balance between ATP depletion after the MPT and ATP generation by glycolysis determines whether the fate of cells will be apoptotic or necrotic death. Thus, the MPT is a common pathway leading to both necrotic and apoptotic cell death after ischemia/reperfusion.

Original languageEnglish
Pages (from-to)463-470
Number of pages8
JournalBiochemical and Biophysical Research Communications
Volume304
Issue number3
DOIs
StatePublished - May 9 2003
Externally publishedYes

Keywords

  • Apoptosis
  • Hepatocytes
  • Ischemia/Reperfusion
  • Mitochondrial permeability transition
  • Necrosis

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