Regulated production of free radicals by the mitochondrial electron transport chain: Cardiac ischemic preconditioning

Satoshi Matsuzaki, Pamela A. Szweda, Luke I. Szweda, Kenneth M. Humphries

Research output: Contribution to journalReview article

20 Scopus citations

Abstract

Excessive production of free radicals by mitochondria is associated with, and likely contributes to, the progression of numerous pathological conditions. Nevertheless, the production of free radicals by the mitochondria may have important biological functions under normal or stressed conditions by activating or modulating redox-sensitive cellular signaling pathways. This raises the intriguing possibility that regulated mitochondrial free radical production occurs via mechanisms that are distinct from pathologies associated with oxidative damage. Indeed, the capacity of mitochondria to produce free radicals in a limited manner may play a role in ischemic preconditioning, the phenomenon whereby short bouts of ischemia protect from subsequent prolonged ischemia and reperfusion. Ischemic preconditioning can thus serve as an important model system for defining regulatory mechanisms that allow for transient, signal-inducing, production of free radicals by mitochondria. Defining how these mechanism(s) occur will provide insight into therapeutic approaches that minimize oxidative damage without altering normal cellular redox biology. The aim of this review is to present and discuss evidence for the regulated production of superoxide by the electron transport chain within the ischemic preconditioning paradigm of redox regulation.

Original languageEnglish (US)
Pages (from-to)1324-1331
Number of pages8
JournalAdvanced Drug Delivery Reviews
Volume61
Issue number14
DOIs
StatePublished - Nov 30 2009

Keywords

  • Cardiac ischemia
  • Electron transport chain
  • Free radicals
  • Mitochondria
  • Oxidation and reduction
  • Preconditioning

ASJC Scopus subject areas

  • Pharmaceutical Science

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