Journal
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Volume 315, Issue 5, Pages H1215-H1231Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.00124.2018
Keywords
cardioprotection; conditioning; connexin43; ischemia-reperfusion; mitochondria; mitochondrial dynamics; mitochondrial permeability transition pore; reactive oxygen species
Funding
- German Research Foundation [BO 2955/4-1]
- Collaborative Research Centre (SFB/CRC) [1213/B05]
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Several interventions, such as ischemic preconditioning, remote pre/perconditioning, or postconditioning, are known to decrease lethal myocardial ischemia-reperfusion injury. While several signal transduction pathways become activated by such maneuvers, they all have a common end point, namely, the mitochondria. These organelles represent an essential target of the cardioprotective strategies, and the preservation of mitochondrial function is central for the reduction of ischemia-reperfusion injury. In the present review, we address the role of mitochondria in the different conditioning strategies; in particular, we focus on alterations of mitochondrial function in terms of energy production, formation of reactive oxygen species, opening of the mitochondrial permeability transition pore, and mitochondrial dynamics induced by ischemia-reperfusion.
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