NADPH oxidase 4 (Nox4) is a major source of oxidative stress in the failing heart
暂无分享,去创建一个
Michael D. Schneider | Tetsuro Ago | Michael D Schneider | J. Sadoshima | P. Zhai | T. Ago | J. Kuroda | S. Matsushima | Shouji Matsushima | Junichi Sadoshima | Peiyong Zhai | Junya Kuroda | M. Schneider | Shouji Matsushima
[1] K. Griendling,et al. Nox proteins in signal transduction. , 2009, Free radical biology & medicine.
[2] M. Hattori,et al. A Novel Superoxide-producing NAD(P)H Oxidase in Kidney* , 2001, The Journal of Biological Chemistry.
[3] B. A. French,et al. Gene recombination in postmitotic cells. Targeted expression of Cre recombinase provokes cardiac-restricted, site-specific rearrangement in adult ventricular muscle in vivo. , 1997, The Journal of clinical investigation.
[4] A. Shah,et al. Activation of NADPH Oxidase During Progression of Cardiac Hypertrophy to Failure , 2002, Hypertension.
[5] M. Ushio-Fukai. Localizing NADPH Oxidase–Derived ROS , 2006, Science's STKE.
[6] A. Takeshita,et al. Direct evidence for increased hydroxyl radicals originating from superoxide in the failing myocardium. , 2000, Circulation research.
[7] G Rotilio,et al. Disulfide relays and phosphorylative cascades: partners in redox-mediated signaling pathways , 2005, Cell Death and Differentiation.
[8] A. Zeiher,et al. A “Reductionist” View of Cardiomyopathy , 2007, Cell.
[9] Hiroyuki Tsutsui,et al. Treatment With Dimethylthiourea Prevents Left Ventricular Remodeling and Failure After Experimental Myocardial Infarction in Mice: Role of Oxidative Stress , 2000, Circulation research.
[10] S. Ibayashi,et al. Nox4 as the Major Catalytic Component of an Endothelial NAD(P)H Oxidase , 2004, Circulation.
[11] Peipei Ping,et al. Role of the mitochondrial permeability transition in myocardial disease. , 2003, Circulation research.
[12] J. Sadoshima,et al. Upregulation of Nox4 by Hypertrophic Stimuli Promotes Apoptosis and Mitochondrial Dysfunction in Cardiac Myocytes , 2010, Circulation research.
[13] Simon J. Walker,et al. NADPH oxidases in cardiovascular health and disease. , 2006, Antioxidants & redox signaling.
[14] Steven J. Sollott,et al. Reactive Oxygen Species (Ros-Induced) Ros Release , 2000, The Journal of experimental medicine.
[15] H. Sumimoto. Structure, regulation and evolution of Nox‐family NADPH oxidases that produce reactive oxygen species , 2008, The FEBS journal.
[16] Pravir Kumar,et al. Direct Interaction of the Novel Nox Proteins with p22phox Is Required for the Formation of a Functionally Active NADPH Oxidase* , 2004, Journal of Biological Chemistry.
[17] A. Shah,et al. Contrasting Roles of NADPH Oxidase Isoforms in Pressure-Overload Versus Angiotensin II–Induced Cardiac Hypertrophy , 2003, Circulation research.
[18] J. Sadoshima,et al. Quantitative analysis of redox-sensitive proteome with DIGE and ICAT. , 2008, Journal of proteome research.
[19] M. Ikeda-Saito,et al. Redox-dependent modulation of aconitase activity in intact mitochondria. , 2003, Biochemistry.
[20] Mark A Sussman,et al. Cardiac Progenitor Cell Cycling Stimulated by Pim-1 Kinase , 2010, Circulation research.
[21] K. Krause,et al. The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology. , 2007, Physiological reviews.
[22] S. Vatner,et al. A Redox-Dependent Pathway for Regulating Class II HDACs and Cardiac Hypertrophy , 2008, Cell.
[23] M. Dinauer,et al. Functional analysis of Nox4 reveals unique characteristics compared to other NADPH oxidases. , 2006, Cellular signalling.
[24] J. Sadoshima. Redox regulation of growth and death in cardiac myocytes. , 2006, Antioxidants & redox signaling.
[25] Masahiro Ito,et al. Pressure Overload–Induced Myocardial Hypertrophy in Mice Does Not Require gp91phox , 2004, Circulation.
[26] P. Singal,et al. Antioxidant changes in hypertrophied and failing guinea pig hearts. , 1994, The American journal of physiology.
[27] Jeffrey Robbins,et al. Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death , 2005, Nature.
[28] A. Takeshita,et al. Mitochondrial electron transport complex I is a potential source of oxygen free radicals in the failing myocardium. , 1999, Circulation research.
[29] A. Shah,et al. Increased myocardial NADPH oxidase activity in human heart failure. , 2003, Journal of the American College of Cardiology.
[30] D. Sorescu,et al. NAD(P)H Oxidase 4 Mediates Transforming Growth Factor-β1–Induced Differentiation of Cardiac Fibroblasts Into Myofibroblasts , 2005, Circulation research.