Manganese Superoxide Dismutase: Guardian of the Heart

Submit Manuscript | http://medcraveonline.com MOJ Anat Physiol 2015, 1(2): 00006 was neonatal lethal. Due to background modifications, a small percentage of knockout mice showed dilated cardiomyopathy indicating increased vulnerability to oxidative injury in the cardiac myocytes [1]. Ikegami et al. [3] successfully generated tissuespecific MnSOD conditional knockout mice that would provide a useful tool for the analysis of the pathophysiological role of O2 [3]. Studies have also been done on heterozygous mice to observe the effect of low MnSOD activity throughout life due to increased oxidative damage, progressing with age [4]. MnSOD has also been shown to play an important role in cardiac tissue protection. A study done in 2005 by Sam et al. [5] on failing myocardium showed increase in mRNA expression but decreased activity of MnSOD, which is consistent with the fact that increased oxidative stress leads to higher production of MnSOD [5]. Another study by Lai et al. showed increased oxidative stress in cardiomyocytes by overexpression of adenylyl cyclase 5 which was mediated by decreased MnSOD transcription. These effects were overcome by overexpression of MnSOD with improved cardiac function [6]. Similarly, signal transducer and activator of transcription 3 (STAT3) protects cardiomyocytes against ROS by up regulating MnSOD [7] in hypoxic cardiomyocyte.