Abstract
Mitochondrial-Targeted Antioxidants Given at Reperfusion Protect Cardiac and Hindlimb Muscles against Ischemia/Reperfusion Injury
Highlights
The incidence of Myocardial Infarction (MI) in the United States is 800,000 annually [2]
The results indicate that mitochondrial-derived Reactive Oxygen Species (ROS) is a major contributor to reperfusion injury and that MitoQ and SS-31 work expeditiously to attenuate ROS in that both agents improve cardiac function and limit infarct size when administered only at the onset of reperfusion
The data suggest that MitoQ or SS-31 would be an effective adjuvant to reduce ischemia reperfusion injury in acute myocardial infarction patients receiving percutaneous coronary intervention, thrombolytic therapy, or undergoing coronary by-pass surgery
Summary
The incidence of Myocardial Infarction (MI) in the United States is 800,000 annually [2]. It is critical to understand the underlying mechanisms to develop effective therapeutic strategies to mitigate I/R induced cardiac damage [4,5]. The principal cause of cardiomyocyte dysfunction and necrosis resulting from Ischemia/Reperfusion (I/R) injury is the production and release of Reactive Oxygen Species (ROS) from damaged mitochondria. Attenuation of I/R-induced ROS production has been a therapeutic strategy to salvage damaged cardiomyocytes and thereby limit cardiac functional impairment and infarct size [1]. This study was undertaken to determine whether these agents are effective in limiting myocardial and hindlimb I/R injury when given during the first 5min of reperfusion only, and thereby support the premise that mitochondrial damage underlies reperfusion-induced cell death during the initial minutes of reperfusion
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