The cardioprotective effects elicited by p66(Shc) ablation demonstrate the crucial role of mitochondrial ROS formation in ischemia/reperfusion injury.
暂无分享,去创建一个
P. Pelicci | M. Giorgio | N. Kaludercic | F. Di Lisa | R. Menabò | A. Carpi | R. Menabò
[1] S. Schiaffino,et al. Cardiac interstitial cells express GATA4 and control dedifferentiation and cell cycle re-entry of adult cardiomyocytes. , 2009, Journal of molecular and cellular cardiology.
[2] M. Giorgio,et al. Mitochondrial pathways for ROS formation and myocardial injury: the relevance of p66Shc and monoamine oxidase , 2009, Basic Research in Cardiology.
[3] Michael P. Murphy,et al. How mitochondria produce reactive oxygen species , 2008, The Biochemical journal.
[4] S. Minucci,et al. p66Shc-generated Oxidative Signal Promotes Fat Accumulation* , 2008, Journal of Biological Chemistry.
[5] J. Stamler,et al. Redox-based regulation of signal transduction: principles, pitfalls, and promises. , 2008, Free radical biology & medicine.
[6] P. Pelicci,et al. The proapoptotic and antimitogenic protein p66SHC acts as a negative regulator of lymphocyte activation and autoimmunity. , 2008, Blood.
[7] T. Lüscher,et al. Final common molecular pathways of aging and cardiovascular disease: role of the p66Shc protein. , 2008, Arteriosclerosis, thrombosis, and vascular biology.
[8] D. Yellon,et al. Myocardial reperfusion injury. , 2007, The New England journal of medicine.
[9] P. Pelicci,et al. Hydrogen peroxide: a metabolic by-product or a common mediator of ageing signals? , 2007, Nature Reviews Molecular Cell Biology.
[10] T. Lüscher,et al. Diabetes Promotes Cardiac Stem Cell Aging and Heart Failure, Which Are Prevented by Deletion of the p66shc Gene , 2006, Circulation research.
[11] S. Menini,et al. Deletion of p66Shc Longevity Gene Protects Against Experimental Diabetic Glomerulopathy by Preventing Diabetes-Induced Oxidative Stress , 2006, Diabetes.
[12] P. Pelicci,et al. Apoptosis and aging: role of p66Shc redox protein. , 2006, Antioxidants & redox signaling.
[13] R. Erbel,et al. Oxidative modification of tropomyosin and myocardial dysfunction following coronary microembolization. , 2006, European heart journal.
[14] E. Masini,et al. Oxidative Stress by Monoamine Oxidase Mediates Receptor-Independent Cardiomyocyte Apoptosis by Serotonin and Postischemic Myocardial Injury , 2005, Circulation.
[15] A. Naqvi,et al. Rac1 leads to phosphorylation-dependent increase in stability of the p66shc adaptor protein: role in Rac1-induced oxidative stress. , 2005, Molecular biology of the cell.
[16] P. Pelicci,et al. Genetic Deletion of the p66Shc Adaptor Protein Protects From Angiotensin II–Induced Myocardial Damage , 2005, Hypertension.
[17] S. Minucci,et al. Electron Transfer between Cytochrome c and p66Shc Generates Reactive Oxygen Species that Trigger Mitochondrial Apoptosis , 2005, Cell.
[18] P. Bernardi,et al. Mitochondrial function and myocardial aging. A critical analysis of the role of permeability transition. , 2005, Cardiovascular research.
[19] D. Pimentel,et al. A new hypertrophic mechanism of serotonin in cardiac myocytes: receptor‐independent ROS generation , 2005, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[20] Robert S. Balaban,et al. Mitochondria, Oxidants, and Aging , 2005, Cell.
[21] P. Pelicci,et al. p66ShcA Modulates Tissue Response to Hindlimb Ischemia , 2004, Circulation.
[22] J. V. Van Eyk,et al. Evidence of myofibrillar protein oxidation induced by postischemic reperfusion in isolated rat hearts. , 2004, American journal of physiology. Heart and circulatory physiology.
[23] P. Pelicci,et al. p66SHC Promotes Apoptosis and Antagonizes Mitogenic Signaling in T Cells , 2004, Molecular and Cellular Biology.
[24] J. Turrens,et al. Mitochondrial formation of reactive oxygen species , 2003, The Journal of physiology.
[25] T. Finkel. Oxidant signals and oxidative stress. , 2003, Current opinion in cell biology.
[26] T. Lüscher,et al. Deletion of p66shc Gene Protects Against Age-Related Endothelial Dysfunction , 2003, Circulation.
[27] D. Newmeyer,et al. Mitochondria Releasing Power for Life and Unleashing the Machineries of Death , 2003, Cell.
[28] C. Napoli,et al. Deletion of the p66Shc longevity gene reduces systemic and tissue oxidative stress, vascular cell apoptosis, and early atherogenesis in mice fed a high-fat diet , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[29] S. Minucci,et al. A p53-p66Shc signalling pathway controls intracellular redox status, levels of oxidation-damaged DNA and oxidative stress-induced apoptosis , 2002, Oncogene.
[30] S. Nemoto,et al. Redox Regulation of Forkhead Proteins Through a p66shc-Dependent Signaling Pathway , 2002, Science.
[31] P. Bernardi,et al. Opening of the Mitochondrial Permeability Transition Pore Causes Depletion of Mitochondrial and Cytosolic NAD+and Is a Causative Event in the Death of Myocytes in Postischemic Reperfusion of the Heart* , 2001, The Journal of Biological Chemistry.
[32] M. Hengartner. The biochemistry of apoptosis , 2000, Nature.
[33] J. Downey,et al. Opening of Mitochondrial KATP Channels Triggers the Preconditioned State by Generating Free Radicals , 2000, Circulation research.
[34] Pier Paolo Pandolfi,et al. The p66shc adaptor protein controls oxidative stress response and life span in mammals , 1999, Nature.
[35] E. Marbán,et al. Molecular and cellular mechanisms of myocardial stunning. , 1999, Physiological reviews.
[36] T. Vanden Hoek,et al. Reactive Oxygen Species Released from Mitochondria during Brief Hypoxia Induce Preconditioning in Cardiomyocytes* , 1998, The Journal of Biological Chemistry.
[37] G. Superti-Furga,et al. Opposite effects of the p52shc/p46shc and p66shc splicing isoforms on the EGF receptor–MAP kinase–fos signalling pathway , 1997, The EMBO journal.
[38] S. Schiaffino,et al. Binding of cytosolic proteins to myofibrils in ischemic rat hearts. , 1996, Circulation research.
[39] T. Pawson,et al. A novel transforming protein (SHC) with an SH2 domain is implicated in mitogenic signal transduction , 1992, Cell.
[40] B. Siegmund,et al. Prevention of the oxygen paradox in hypoxic-reoxygenated hearts. , 1991, The American journal of physiology.
[41] K. Yagi,et al. Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction. , 1979, Analytical biochemistry.
[42] J. Downey,et al. Redox signaling at reperfusion is required for protection from ischemic preconditioning but not from a direct PKC activator , 2007, Basic Research in Cardiology.
[43] W. Dröge. Free radicals in the physiological control of cell function. , 2002, Physiological reviews.
[44] J. Downey,et al. Free radicals and their involvement during long-term myocardial ischemia and reperfusion. , 1990, Annual review of physiology.
[45] Steven J. Steindel,et al. 4 Lactate Dehydrogenase , 1975 .