Inhibition of RIP1-dependent necrosis prevents adverse cardiac remodeling after myocardial ischemia–reperfusion in vivo
暂无分享,去创建一个
[1] P. Doevendans,et al. Targeting cell death in the reperfused heart: pharmacological approaches for cardioprotection. , 2013, International journal of cardiology.
[2] P. Doevendans,et al. Human versus porcine mesenchymal stromal cells: phenotype, differentiation potential, immunomodulation and cardiac improvement after transplantation , 2012, Journal of cellular and molecular medicine.
[3] Ji Luo,et al. Mixed lineage kinase domain-like is a key receptor interacting protein 3 downstream component of TNF-induced necrosis , 2012, Proceedings of the National Academy of Sciences.
[4] Xiaodong Wang,et al. Mixed Lineage Kinase Domain-like Protein Mediates Necrosis Signaling Downstream of RIP3 Kinase , 2012, Cell.
[5] G. Kung,et al. Programmed necrosis, not apoptosis, in the heart. , 2011, Circulation research.
[6] L. Martin,et al. Necrostatin Decreases Oxidative Damage, Inflammation, and Injury after Neonatal HI , 2011, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[7] Xuehui Liu,et al. Trimetazidine inhibits pressure overload-induced cardiac fibrosis through NADPH oxidase-ROS-CTGF pathway. , 2010, Cardiovascular research.
[8] P. Vandenabeele,et al. Molecular mechanisms of necroptosis: an ordered cellular explosion , 2010, Nature Reviews Molecular Cell Biology.
[9] H. Bøtker,et al. Translating novel strategies for cardioprotection: the Hatter Workshop Recommendations , 2010, Basic Research in Cardiology.
[10] G. Heusch,et al. TNFalpha in atherosclerosis, myocardial ischemia/reperfusion and heart failure. , 2010, Pharmacology & therapeutics.
[11] M. Goumans,et al. MicroRNA-155 prevents necrotic cell death in human cardiomyocyte progenitor cells via targeting RIP1 , 2010, Journal of cellular and molecular medicine.
[12] Akio Matsumoto,et al. Biochemistry and physiology of mitochondrial ion channels involved in cardioprotection , 2010, FEBS letters.
[13] M. Goumans,et al. Active Wnt signaling in response to cardiac injury , 2010, Basic Research in Cardiology.
[14] T. Vanden Berghe,et al. The Role of the Kinases RIP1 and RIP3 in TNF-Induced Necrosis , 2010, Science Signaling.
[15] D. Mozaffarian,et al. Heart disease and stroke statistics--2010 update: a report from the American Heart Association. , 2010, Circulation.
[16] R. Kitsis,et al. Cell death in the pathogenesis of heart disease: mechanisms and significance. , 2010, Annual review of physiology.
[17] Xiangbin Xu,et al. Direct relationship between levels of TNF-α expression and endothelial dysfunction in reperfusion injury , 2010, Basic Research in Cardiology.
[18] G. Heusch,et al. Inhibition of mitochondrial permeability transition pore opening: the holy grail of cardioprotection , 2010, Basic Research in Cardiology.
[19] P. Doevendans,et al. Myocardial Ischemia / Reperfusion Injury Is Mediated by Leukocytic Toll-Like Receptor-2 and Reduced by Systemic Administration of a Novel Anti – Toll-Like Receptor-2 Antibody , 2009 .
[20] O. Carretero,et al. Lack of Glutathione Peroxidase 1 Accelerates Cardiac-Specific Hypertrophy and Dysfunction in Angiotensin II Hypertension , 2010, Hypertension.
[21] B. Gersh,et al. Reperfusion Injury, Microvascular Dysfunction, and Cardioprotection: The “Dark Side” of Reperfusion , 2009, Circulation.
[22] R. Erbel,et al. Coronary microembolization: from bedside to bench and back to bedside. , 2009, Circulation.
[23] L. Papucci,et al. Role of NADPH oxidase in H9c2 cardiac muscle cells exposed to simulated ischaemia‐reperfusion , 2009, Journal of cellular and molecular medicine.
[24] Na Zhang,et al. RIP3, an Energy Metabolism Regulator That Switches TNF-Induced Cell Death from Apoptosis to Necrosis , 2009, Science.
[25] Tao Wang,et al. Receptor Interacting Protein Kinase-3 Determines Cellular Necrotic Response to TNF-α , 2009, Cell.
[26] F. Chan,et al. Phosphorylation-Driven Assembly of the RIP1-RIP3 Complex Regulates Programmed Necrosis and Virus-Induced Inflammation , 2009, Cell.
[27] Yuyuan Han,et al. Gαi1 and Gαi3 Are Required for Epidermal Growth Factor–Mediated Activation of the Akt-mTORC1 Pathway , 2009, Science Signaling.
[28] D. Yellon,et al. The mitochondrial permeability transition pore as a target for preconditioning and postconditioning , 2009, Basic Research in Cardiology.
[29] C. Baines. The mitochondrial permeability transition pore and ischemia-reperfusion injury , 2009, Basic Research in Cardiology.
[30] E. Murphy,et al. Cardioprotection and altered mitochondrial adenine nucleotide transport , 2009, Basic Research in Cardiology.
[31] L. Boscá,et al. Constitutive COX-2 activity in cardiomyocytes confers permanent cardioprotection Constitutive COX-2 expression and cardioprotection. , 2009, Journal of molecular and cellular cardiology.
[32] G. Heusch,et al. Cardioprotection: nitric oxide, protein kinases, and mitochondria. , 2008, Circulation.
[33] M. Moskowitz,et al. Necrostatin-1 Reduces Histopathology and Improves Functional Outcome after Controlled Cortical Impact in Mice , 2008, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[34] Alexei Degterev,et al. Identification of RIP1 kinase as a specific cellular target of necrostatins. , 2008, Nature chemical biology.
[35] You-Sun Kim,et al. TNFα and reactive oxygen species in necrotic cell death , 2008, Cell Research.
[36] Richard T. Lee,et al. Targeted Deletion of Thioredoxin-Interacting Protein Regulates Cardiac Dysfunction in Response to Pressure Overload , 2007, Circulation research.
[37] M. Mocanu,et al. The Cardioprotective Effect of Necrostatin Requires the Cyclophilin-D Component of the Mitochondrial Permeability Transition Pore , 2007, Cardiovascular Drugs and Therapy.
[38] R. Bolli,et al. Cardioprotection Afforded by Inducible Nitric Oxide Synthase Gene Therapy Is Mediated by Cyclooxygenase-2 via a Nuclear Factor-&kgr;B-Dependent Pathway , 2007, Circulation.
[39] D. Yellon,et al. Myocardial reperfusion injury. , 2007, The New England journal of medicine.
[40] D. Yellon,et al. Necrostatin: A Potentially Novel Cardioprotective Agent? , 2007, Cardiovascular Drugs and Therapy.
[41] T. Kodama,et al. Gab family proteins are essential for postnatal maintenance of cardiac function via neuregulin-1/ErbB signaling. , 2007, The Journal of clinical investigation.
[42] S. Sollott,et al. Mitochondrial ROS-induced ROS release: an update and review. , 2006, Biochimica et biophysica acta.
[43] H. Osada,et al. Inhibition of ADP/ATP Exchange in Receptor-Interacting Protein-Mediated Necrosis , 2006, Molecular and Cellular Biology.
[44] H. Krum,et al. Catalytic Degradation of Vitamin D Up-regulated Protein 1 mRNA Enhances Cardiomyocyte Survival and Prevents Left Ventricular Remodeling after Myocardial Ischemia* , 2005, Journal of Biological Chemistry.
[45] Alexei Degterev,et al. Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury , 2005, Nature chemical biology.
[46] J. Vinten-johansen. Involvement of neutrophils in the pathogenesis of lethal myocardial reperfusion injury. , 2004, Cardiovascular research.
[47] J. Turrens,et al. Mitochondrial formation of reactive oxygen species , 2003, The Journal of physiology.
[48] R. Gottlieb. Mitochondrial signaling in apoptosis: Mitochondrial daggers to the breaking heart , 2003, Basic Research in Cardiology.
[49] A. Shah,et al. Increased myocardial NADPH oxidase activity in human heart failure. , 2003, Journal of the American College of Cardiology.
[50] D. Yellon,et al. The mitochondrial permeability transition pore: its fundamental role in mediating cell death during ischaemia and reperfusion. , 2003, Journal of molecular and cellular cardiology.
[51] R. Jackson,et al. Reactive species mechanisms of cellular hypoxia-reoxygenation injury. , 2002, American journal of physiology. Cell physiology.
[52] 塩見 哲也. Overexpression of glutathione peroxidase prevents left ventricular remodeling and failure after myocardial infarction in mice , 2005 .