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Related Experiment Videos

Apoptosis: checkpoint at the mitochondrial frontier.

E Bossy-Wetzel1, D R Green

  • 1Division of Cellular Immunology, La Jolla Institute for Allergy and Immunology, San Diego, CA 92121, USA. ella_bossy@liai.org, ebossyw1@san.rr.com

Mutation Research
|September 16, 1999
PubMed
Summary

Mitochondria play a key role in apoptosis, a regulated cell death process. Cytochrome c release from mitochondria triggers caspase activation, initiating programmed cell death pathways.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Apoptosis is a fundamental, evolutionarily conserved process of programmed cell death.
  • Caspases, a family of cysteine proteases, are central executioners of apoptosis, cleaving cellular substrates.
  • Caspases exist as inactive zymogens and require activation by pro-apoptotic stimuli.

Purpose of the Study:

  • To review recent advances in understanding the role of mitochondria in apoptosis.
  • To elucidate the critical involvement of cytochrome c in initiating the caspase cascade.
  • To discuss the regulatory mechanisms of apoptosis involving Bcl-2 family proteins.

Main Methods:

  • This review synthesizes current research findings on mitochondrial involvement in apoptosis.

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  • It examines the molecular interactions between cytochrome c, Apaf-1, and caspases.
  • The role of the anti-apoptotic protein Bcl-2 in regulating mitochondrial outer membrane permeabilization is discussed.

    • Main Results:

    • Mitochondria are critical regulators of apoptosis, releasing cytochrome c upon apoptotic stimuli.
    • Cytochrome c release facilitates the formation of the apoptosome complex, activating initiator caspase-9.
    • Activated caspase-9 subsequently triggers downstream effector caspases, leading to cell death.

    Conclusions:

    • Mitochondria and cytochrome c are central players in the intrinsic pathway of apoptosis.
    • The release of cytochrome c is a key event that commits the cell to die.
    • Understanding these pathways offers insights into therapeutic strategies for diseases involving aberrant apoptosis.