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Updated: Jul 11, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Targeting cell death

D J Hausenloy1, L Scorrano

  • 1The Hatter Cardiovascular Institute, University College London Hospital, London, UK.

Clinical Pharmacology and Therapeutics
|September 14, 2007
PubMed

Insights

Preventing cell death is key for treating ischemia-reperfusion injury. Targeting mitochondria, crucial in apoptosis, offers novel therapeutic strategies by modulating inner membrane permeability and morphology.

Area of Science:

  • Cardiovascular Science
  • Neuroscience
  • Cell Biology

Background:

  • Myocardial and cerebral infarction lead to significant functional deficits due to excessive cell death.
  • Ischemia-reperfusion injury necessitates therapeutic strategies focused on preventing cell death.

Purpose of the Study:

  • To highlight the critical role of mitochondria in ischemia-reperfusion.
  • To identify mitochondrial inner membrane permeability and morphology as potential therapeutic targets.

Main Methods:

  • Review of existing literature on cell death mechanisms in ischemia-reperfusion.
  • Analysis of the role of mitochondria in apoptotic pathways.

Main Results:

  • Mitochondria are central amplifiers of apoptotic cascades during ischemia-reperfusion.
  • Alterations in mitochondrial inner membrane permeability and morphology are key regulated processes.

Conclusions:

  • Modulating mitochondrial function presents a promising therapeutic avenue for ischemia-reperfusion injury.
  • Targeting mitochondrial changes could reduce cell death and improve outcomes in infarction.

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