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Mitochondria in Cardiac Postconditioning.

Pasquale Pagliaro1, Saveria Femminò1, Jasmin Popara1

  • 1Department of Clinical and Biological Sciences, University of Turin, Turin, Italy.

Frontiers in Physiology
|April 11, 2018
PubMed
Summary
This summary is machine-generated.

Mitochondria are key to heart protection. This review explores how mitochondrial parts like connexin 43 and KATP channels aid cardiac postconditioning, limiting cell death and aiding clinical translation.

Keywords:
cardioprotectionconnexin 43ischemia/reperfusionmitochondriareactive oxygen speciesredox signaling

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Area of Science:

  • Cardiovascular Science
  • Mitochondrial Biology
  • Cellular Physiology

Background:

  • Mitochondria are crucial for cardioprotection.
  • Postconditioning is a protective strategy against cardiac injury.
  • Mitochondrial components are implicated in cardioprotective signaling.

Purpose of the Study:

  • To review the historical role of mitochondrial mechanisms in cardiac postconditioning.
  • To discuss key mitochondrial components involved in postconditioning.
  • To explore the link between mitochondrial signaling and cell death limitation.

Main Methods:

  • Literature review of fundamental studies on mitochondrial components in postconditioning.
  • Discussion of reactive oxygen species, gaseous molecules, and anesthetics in postconditioning.
  • Analysis of mitochondrial postconditioning signaling pathways.

Main Results:

  • Connexin 43, mitochondrial KATP channels, and the mitochondrial permeability transition pore are central to postconditioning.
  • Mitochondrial signaling pathways are critical for limiting cell death.
  • Reactive oxygen species and gaseous molecules modulate postconditioning effects.

Conclusions:

  • Mitochondrial mechanisms are fundamental to cardiac postconditioning.
  • Understanding these mechanisms is vital for clinical translation.
  • Further research into mitochondrial signaling can improve cardioprotective strategies.