Zinc and myocardial ischemia/reperfusion injury

Biometals. 2013 Dec;26(6):863-78. doi: 10.1007/s10534-013-9671-x. Epub 2013 Aug 28.


As an important trace element, zinc is required for the normal cellular structure and function, and impairment of zinc homeostasis is associated with a variety of health problems including cardiovascular disease. Zinc homeostasis is regulated through zinc transporters, zinc binding molecules, and zinc sensors. Zinc also plays a critical role in cellular signaling. Studies have documented that zinc homeostasis is impaired by ischemia/reperfusion in the heart and zinc dyshomeostasis may play a role in the pathogenesis of myocardial ischemia/reperfusion injury. Both exogenous and endogenously released zinc may play an important role in cardioprotection against ischemia/reperfusion injury. The goal of this review is to summarize the current understanding of the roles of zinc homeostasis and zinc signaling in myocardial ischemia/reperfusion injury.

Publication types

  • Review

MeSH terms

  • Biological Transport
  • Cation Transport Proteins / genetics
  • Cation Transport Proteins / metabolism*
  • Gene Expression Regulation
  • Homeostasis
  • Humans
  • Metallothionein / genetics
  • Metallothionein / metabolism
  • Myocardial Reperfusion Injury / genetics
  • Myocardial Reperfusion Injury / metabolism*
  • Myocardial Reperfusion Injury / pathology
  • Myocardium / metabolism*
  • Myocardium / pathology
  • Protein Kinases / genetics
  • Protein Kinases / metabolism
  • Signal Transduction
  • Zinc / metabolism*


  • Cation Transport Proteins
  • Metallothionein
  • Protein Kinases
  • Zinc