Mechanisms by which hydrogen sulfide attenuates muscle function following ischemia-reperfusion injury: Effects on Akt signaling, mitochondrial function, and apoptosis

Michael D. Wetzel, Joseph C. Wenke

Research output: Contribution to journalReview articlepeer-review

11 Scopus citations

Abstract

Ischemia-reperfusion injury is caused by a period of ischemia followed by massive blood flow into a tissue that had experienced restricted blood flow. The severity of the injury is dependent on the time the tissue was restricted from blood flow, becoming more severe after longer ischemia times. This can lead to many complications such as tissue necrosis, cellular apoptosis, inflammation, metabolic and mitochondrial dysfunction, and even organ failure. One of the emerging therapies to combat ischemic reperfusion injury complications is hydrogen sulfide, which is a gasotransmitter that diffuses across cell membranes to exert effects on various signaling pathways regulating cell survival such as Akt, mitochondrial activity, and apoptosis. Although commonly thought of as a toxic gas, low concentrations of hydrogen sulfide have been shown to be beneficial in promoting tissue survival post-ischemia, and modulate a wide variety of cellular responses. This review will detail the mechanisms of hydrogen sulfide in affecting the Akt signaling pathway, mitochondrial function, and apoptosis, particularly in regards to ischemic reperfusion injury in muscle tissue. It will conclude with potential clinical applications of hydrogen sulfide, combinations with other therapies, and perspectives for future studies.

Original languageEnglish (US)
Article number33
JournalJournal of Translational Medicine
Volume17
Issue number1
DOIs
StatePublished - Jan 21 2019
Externally publishedYes

Keywords

  • Akt
  • Apoptosis
  • eNOS
  • Hydrogen sulfide
  • Ischemia reperfusion injury
  • Mitochondria
  • Muscle

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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