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10.1016/j.gde.2016.03.001 http://scihub22266oqcxt.onion/10.1016/j.gde.2016.03.001 C5055416!5055416!27061490     free     free     free       Curr+Opin+Genet+Dev 2016 ; 38 (ä): 38-44 Nephropedia Template TP {{tp|p=27061490|t=2016. Mitochondrial fission/fusion and cardiomyopathy |pdf=|usr=}}{{27061490}} gab.com Text Mitochondrial fission/fusion and cardiomyopathy JO: Curr Opin Genet Dev http://www.kidney.de/pget.php?&tw=1&pmid=27061490 #FOAvip Mitochondria are highly abundant in and essential to the beat-to-beat contractile performance of hearts. However, relatively few cardiac diseases have been attributed to primary mitochondrial dysfunction. The paucity of evidence for ?primary mitochondrial cardiac diseases? may be because such an entity doesn?t exist. Alternately, the consequences of mitochondrial dysfunction on hearts may be so severe that long-term viability is severely impaired and affected individuals are therefore not included in standard genetic screens of adult heart disease subjects. Here, I review accumulating experimental evidence that impairing mitochondrial fission or fusion causes cardiomyopathy in otherwise normal mice, and consider how these data could motivate screening of perinatal cardiomyopathy subjects for damaging mutations of mitochondrial fission and fusion factors. Twit Text FOAVip Mitochondrial fission/fusion and cardiomyopathy ????Curr Opin Genet Dev http://www.kidney.de/pget.php?&tw=1&pmid=27061490 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27061490 #FOAvip English Wikipedia <ref>{{Cite pmid|27061490}}</ref> Mitochondrial fission/fusion and cardiomyopathy #MMPMID27061490 Dorn GW Curr Opin Genet Dev 2016[Jun]; 38 (ä): 38-44 PMID27061490show ga Mitochondria are highly abundant in and essential to the beat-to-beat contractile performance of hearts. However, relatively few cardiac diseases have been attributed to primary mitochondrial dysfunction. The paucity of evidence for ?primary mitochondrial cardiac diseases? may be because such an entity doesn?t exist. Alternately, the consequences of mitochondrial dysfunction on hearts may be so severe that long-term viability is severely impaired and affected individuals are therefore not included in standard genetic screens of adult heart disease subjects. Here, I review accumulating experimental evidence that impairing mitochondrial fission or fusion causes cardiomyopathy in otherwise normal mice, and consider how these data could motivate screening of perinatal cardiomyopathy subjects for damaging mutations of mitochondrial fission and fusion factors. äMitochondrial fission/fusion and cardiomyopathy (epmc).pdf DeepDyve Pubget Overpricing