Abstract
Mitochondria are key regulators of cell fate through controlling ATP generation and releasing pro-apoptotic factors. Cardiac ischemia/reperfusion (I/R) injury to the coronary microcirculation has manifestations ranging in severity from reversible edema to interstitial hemorrhage. A number of mechanisms have been proposed to explain the cardiac microvascular I/R injury including edema, impaired vasomotion, coronary microembolization, and capillary destruction. In contrast to their role in cell types with higher energy demands, mitochondria in endothelial cells primarily function in signaling cellular responses to environmental cues. It is clear that abnormal mitochondrial signatures, including mitochondrial oxidative stress, mitochondrial fission, mitochondrial fusion, and mitophagy, play a substantial role in endothelial cell function. While the pathogenic role of each of these mitochondrial alterations in the endothelial cells I/R injury remains complex, profiling of mitochondrial oxidative stress and mitochondrial dynamics in endothelial cell dysfunction may offer promising potential targets in the search for novel diagnostics and therapeutics in cardiac microvascular I/R injury. The objective of this review is to discuss the role of mitochondrial oxidative stress on cardiac microvascular endothelial cells dysfunction. Mitochondrial dynamics, including mitochondrial fission and fusion, are critically discussed to understand their roles in endothelial cell survival. Finally, mitophagy, as a degradative mechanism for damaged mitochondria, is summarized to figure out its contribution to the progression of microvascular I/R injury.
Highlights
Acute myocardial infarction (AMI) is caused by blockage of one or more of the coronary arteries that supply the heart [1,2]
Administration of reactive oxygen species (ROS) scavenger TEMPOL leads to a significant decrease in mitochondrial fragmentation without altering the levels of Optic atrophy 1 (Opa1) [162]. These results indicate that mitochondrial fusion may play a protective role in regulating endothelial cell function
It is increasingly appreciated that mitochondria serve as the sentinel organelles that are capable of detecting insult signals and orchestrating inflammation responses [195,196]
Summary
Acute myocardial infarction (AMI) is caused by blockage of one or more of the coronary arteries that supply the heart [1,2]. Patients that received reperfusion strategies including growth factor (VEGF) and adhesion molecule are expressed on the surface of endothelial cells and percutaneous transluminal coronary intervention or coronary artery bypass grafting surgery [21,22]. Unlike that mitochondria cells mitochondria-dependent mainly play a prominent role production in signalingis cellular cardiomyocytesinorendothelial skeletal muscle, energy relativelyresponses low in to vascular endothelium, which uses glycolysis to produce. It is environmental cues [34,35]. The low mitochondrial content in endothelial cells further validates a non-canonical function to stress, reactive oxygen species (ROS) are produced by mitochondria and employed as a second played by mitochondria in regulating signaling responses rather than in glucose metabolism [37]. Mitochondrial dynamics in cardiac microvascular I/R injury (Figure 1)
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