Mitochondria: Mitochondrial participation in ischemia-reperfusion injury in skeletal muscle

Anne Lejay, Alain Meyer, Anna Isabel Schlagowski, Anne Laure Charles, François Singh, Jamal Bouitbir, Julien Pottecher, Nabil Chakfé, Joffrey Zoll, Bernard Geny

Research output: Contribution to journalShort surveypeer-review

63 Scopus citations

Abstract

Irrespective of the organ involved, restoration of blood flow to ischemic tissue is vital, although reperfusion per se is deleterious. In the setting of vascular surgery, even subtle skeletal muscle ischemia contributes to remote organ injuries and perioperative and long-term morbidities. Reperfusion-induced injury is thought to participate in up to 40% of muscle damage. Recently, the pathophysiology of lower limb ischemia-reperfusion (IR) has been largely improved, acknowledging a key role for mitochondrial dysfunction mainly characterized by impaired mitochondrial oxidative capacity and premature mitochondrial permeability transition pore opening. Increased oxidative stress triggered by an imbalance between reactive oxygen species (ROS) production and clearance, and facilitated by enhanced inflammation, appears to be both followed and instigated by mitochondrial dysfunction. Mitochondria are both actors and target of IR and therapeutic strategies modulating degree of ROS production could enhance protective signals and allow for mitochondrial protection through a mitohormesis mechanism.

Original languageEnglish (US)
Pages (from-to)101-105
Number of pages5
JournalInternational Journal of Biochemistry and Cell Biology
Volume50
Issue number1
DOIs
StatePublished - May 2014

Keywords

  • Ischemia-reperfusion
  • Mitochondria
  • Muscle conditioning
  • Oxidative stress
  • Vascular disease

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology

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