Redox signaling and protein phosphorylation in mitochondria: progress and prospects.
As we learn more about the factors that govern cardiac mitochondrial bioenergetics, fission and fusion, as well as the triggers of apoptotic and necrotic cell death, there is growing appreciation that these dynamic processes are finely-tuned by equally dynamic post-translational modification of proteins in and around the mitochondrion. In this minireview, we discuss the evidence that S-nitrosylation, glutathionylation and phosphorylation of mitochondrial proteins have important bioenergetic consequences. A full accounting of these targets, and the functional impact of their modifications, will be necessary to determine the extent to which these processes underlie ischemia/reperfusion injury, cardioprotection by pre/post-conditioning, and the pathogenesis of heart failure.
Division of Cardiology, Department of Medicine, The Johns Hopkins University School of Medicine, Ross Research Building, Room 847, 720 Rutland Avenue, Baltimore, MD 21205, USA. dbrianfoster@jhmi.edu
D Brian
DB
Foster
Jennifer E
JE
Van Eyk
Eduardo
E
Marbán
Brian
B
O'Rourke
D000818:Animals; D017209:Apoptosis; D006333:Heart Failure / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D019157:Ischemic Preconditioning, Myocardial; D008929:Mitochondria, Heart / Q000378:metabolism* / Q000473:pathology; D024101:Mitochondrial Proteins / Q000378:metabolism*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000473:pathology; D009336:Necrosis; D010084:Oxidation-Reduction; D010766:Phosphorylation; D011499:Protein Processing, Post-Translational
D024101:Mitochondrial Proteins