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Mitochondrial outer membrane permeabilization during apoptosis: the role of mitochondrial fission

Thomas Landes1, Jean-Claude Martinou

  • 1Department of Cell Biology, University of Geneva, Sciences III, 30 quai Ernest Ansermet, 1211 Geneva 4, Switzerland.

Biochimica Et Biophysica Acta
|February 1, 2011
PubMed

Insights

Mitochondria fragment during apoptosis, a process involving outer membrane permeabilization. This review explores mechanisms linking mitochondrial fission and fusion to cell death, clarifying their role in apoptosis.

Area of Science:

  • Cell Biology
  • Mitochondrial Dynamics
  • Apoptosis Research

Background:

  • Mitochondria form a dynamic network through fusion and fission.
  • Apoptosis involves mitochondrial outer membrane permeabilization (MOMP) and cytochrome c release.
  • Mitochondrial fragmentation is observed during apoptosis, but its physiological role is debated.

Purpose of the Study:

  • To review recent advances in understanding mitochondrial fragmentation during apoptosis.
  • To describe the mechanisms underlying mitochondrial fission and fusion in apoptosis.
  • To discuss the interplay between mitochondrial dynamics and the Bax protein in triggering MOMP.

Main Methods:

  • Literature review of current research on mitochondrial dynamics and apoptosis.
  • Analysis of mechanisms controlling mitochondrial fission and fusion.
  • Discussion of the role of Bax in mitochondrial outer membrane permeabilization.

Main Results:

  • Mitochondria undergo massive fission during apoptosis, forming small, round organelles.
  • Mitochondrial elongation and hyperfusion can precede fission, potentially acting as a defense mechanism.
  • Mechanisms of mitochondrial fragmentation may cooperate with Bax to induce MOMP.

Conclusions:

  • Mitochondrial fragmentation is a significant event during apoptosis.
  • Understanding the mechanisms of mitochondrial dynamics is crucial for elucidating apoptosis.
  • Further research is needed to fully clarify the role of mitochondrial fragmentation in cell death pathways.

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