Regulation of cardiac hypertrophy by intracellular signalling pathways
暂无分享,去创建一个
[1] E. Olson,et al. Suppression of Class I and II Histone Deacetylases Blunts Pressure-Overload Cardiac Hypertrophy , 2006, Circulation.
[2] H. Rockman,et al. JNK1 is required to preserve cardiac function in the early response to pressure overload. , 2006, Biochemical and biophysical research communications.
[3] P. Pfluger,et al. Modulatory calcineurin-interacting proteins 1 and 2 function as calcineurin facilitators in vivo. , 2006, Proceedings of the National Academy of Sciences of the United States of America.
[4] Robert D. Gerard,et al. The Transcriptional Coactivator CAMTA2 Stimulates Cardiac Growth by Opposing Class II Histone Deacetylases , 2006, Cell.
[5] Anthony J. Muslin,et al. Akt1 Is Required for Physiological Cardiac Growth , 2006, Circulation.
[6] B. Aronow,et al. Myocyte Enhancer Factors 2A and 2C Induce Dilated Cardiomyopathy in Transgenic Mice* , 2006, Journal of Biological Chemistry.
[7] R. Schwartz,et al. Cardiac-Specific Deletion of Gata4 Reveals Its Requirement for Hypertrophy, Compensation, and Myocyte Viability , 2006, Circulation research.
[8] Tong Zhang,et al. Local InsP3-dependent perinuclear Ca2+ signaling in cardiac myocyte excitation-transcription coupling. , 2006, The Journal of clinical investigation.
[9] J. Molkentin. Dichotomy of Ca2+ in the heart: contraction versus intracellular signaling. , 2006, The Journal of clinical investigation.
[10] Anne M Deschamps,et al. Pathways of matrix metalloproteinase induction in heart failure: bioactive molecules and transcriptional regulation. , 2006, Cardiovascular research.
[11] M. Jeong,et al. Inhibition of Histone Deacetylation Blocks Cardiac Hypertrophy Induced by Angiotensin II Infusion and Aortic Banding , 2005, Circulation.
[12] J. Guan,et al. Inactivation of focal adhesion kinase in cardiomyocytes promotes eccentric cardiac hypertrophy and fibrosis in mice. , 2005, The Journal of clinical investigation.
[13] E. Olson,et al. Control of cardiac growth by histone acetylation/deacetylation. , 2005, Circulation research.
[14] S. Houser,et al. Nuclear Targeting of Akt Enhances Ventricular Function and Myocyte Contractility , 2005, Circulation research.
[15] I. Cohen,et al. A Transgenic Mouse Model of Heart Failure Using Inducible Gαq* , 2005, Journal of Biological Chemistry.
[16] J. Molkentin,et al. Temporally Controlled Onset of Dilated Cardiomyopathy Through Disruption of the SRF Gene in Adult Heart , 2005, Circulation.
[17] R. DePinho,et al. Class IA Phosphoinositide 3-Kinase Regulates Heart Size and Physiological Cardiac Hypertrophy , 2005, Molecular and Cellular Biology.
[18] T. Hewett,et al. Genetic Inhibition or Activation of JNK1/2 Protects the Myocardium from Ischemia-Reperfusion-induced Cell Death in Vivo* , 2005, Journal of Biological Chemistry.
[19] I. Shiojima,et al. Disruption of coordinated cardiac hypertrophy and angiogenesis contributes to the transition to heart failure. , 2005, The Journal of clinical investigation.
[20] M. Drazner,et al. Does load-induced ventricular hypertrophy progress to systolic heart failure? , 2005, American journal of physiology. Heart and circulatory physiology.
[21] M. Baccarini. Second nature: Biological functions of the Raf‐1 “kinase” , 2005, FEBS letters.
[22] R. Dietz,et al. Requirement of Nuclear Factor-&kgr;B in Angiotensin II– and Isoproterenol-Induced Cardiac Hypertrophy In Vivo , 2005, Circulation.
[23] Guy Salama,et al. Calmodulin kinase II inhibition protects against structural heart disease , 2005, Nature Medicine.
[24] G. Dorn,et al. Protein kinase cascades in the regulation of cardiac hypertrophy. , 2005, The Journal of clinical investigation.
[25] J. Molkentin,et al. Direct and Indirect Interactions between Calcineurin-NFAT and MEK1-Extracellular Signal-Regulated Kinase 1/2 Signaling Pathways Regulate Cardiac Gene Expression and Cellular Growth , 2005, Molecular and Cellular Biology.
[26] Matthew Loose,et al. The roles of GATA-4, -5 and -6 in vertebrate heart development. , 2005, Seminars in cell & developmental biology.
[27] P. Caroni,et al. Attenuation of cardiac remodeling after myocardial infarction by muscle LIM protein-calcineurin signaling at the sarcomeric Z-disc. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[28] D. Kass,et al. Chronic inhibition of cyclic GMP phosphodiesterase 5A prevents and reverses cardiac hypertrophy , 2005, Nature Medicine.
[29] K. Lorenz,et al. The transcriptional repressor Nab1 is a specific regulator of pathological cardiac hypertrophy , 2004, Nature Medicine.
[30] 河野 俊一. Blockade of NF-κB ameliorates myocardial hypertrophy in response to chronic infusion of angiotensin 2 , 2005 .
[31] J. Miyazaki,et al. Mitogen-Activated Protein Kinase Plays a Critical Role in Cardiomyocyte Survival but Not in Cardiac Hypertrophic Growth in Response to Pressure Overload , 2004 .
[32] A. Ho,et al. Role of histone deacetylase inhibitors in the treatment of cancer (Review). , 2004, International journal of oncology.
[33] E. Olson,et al. Mice lacking calsarcin-1 are sensitized to calcineurin signaling and show accelerated cardiomyopathy in response to pathological biomechanical stress , 2004, Nature Medicine.
[34] R. Hobbs. Guidelines for the diagnosis and management of heart failure. , 2004, American journal of therapeutics.
[35] M. Sano,et al. Cyclin-Dependent Kinase-9 An RNAPII Kinase at the Nexus of Cardiac Growth and Death Cascades , 2004 .
[36] Da-Zhi Wang,et al. Atrogin-1/muscle atrophy F-box inhibits calcineurin-dependent cardiac hypertrophy by participating in an SCF ubiquitin ligase complex. , 2004, The Journal of clinical investigation.
[37] David L. Williams,et al. NF-κB activation is required for the development of cardiac hypertrophy in vivo , 2004 .
[38] J. Molkentin,et al. Calcium-calcineurin signaling in the regulation of cardiac hypertrophy. , 2004, Biochemical and biophysical research communications.
[39] Rick B. Vega,et al. Protein Kinases C and D Mediate Agonist-Dependent Cardiac Hypertrophy through Nuclear Export of Histone Deacetylase 5 , 2004, Molecular and Cellular Biology.
[40] E. Olson,et al. Histone Deacetylases 5 and 9 Govern Responsiveness of the Heart to a Subset of Stress Signals and Play Redundant Roles in Heart Development , 2004, Molecular and Cellular Biology.
[41] J. Molkentin. Calcineurin-NFAT signaling regulates the cardiac hypertrophic response in coordination with the MAPKs. , 2004, Cardiovascular research.
[42] C. Proud. Ras, PI3-kinase and mTOR signaling in cardiac hypertrophy. , 2004, Cardiovascular research.
[43] Anthony J. Muslin,et al. Raf-1 Kinase Is Required for Cardiac Hypertrophy and Cardiomyocyte Survival in Response to Pressure Overload , 2004, Circulation.
[44] L. Silengo,et al. PI3Kγ Modulates the Cardiac Response to Chronic Pressure Overload by Distinct Kinase-Dependent and -Independent Effects , 2004, Cell.
[45] M. Crackower,et al. The role of phosphoinositide-3 kinase and PTEN in cardiovascular physiology and disease. , 2004, Journal of molecular and cellular cardiology.
[46] J. Blenis,et al. Deletion of Ribosomal S6 Kinases Does Not Attenuate Pathological, Physiological, or Insulin-Like Growth Factor 1 Receptor-Phosphoinositide 3-Kinase-Induced Cardiac Hypertrophy , 2004, Molecular and Cellular Biology.
[47] S. Izumo,et al. Inhibition of mTOR Signaling With Rapamycin Regresses Established Cardiac Hypertrophy Induced by Pressure Overload , 2004, Circulation.
[48] S. Kudoh,et al. Mechanical stress activates angiotensin II type 1 receptor without the involvement of angiotensin II , 2004, Nature Cell Biology.
[49] D. König,et al. Ausdauersport und kardiale Adaptation (Sportherz) , 2004, Herz.
[50] Stefano Fumagalli,et al. S6K1−/−/S6K2−/− Mice Exhibit Perinatal Lethality and Rapamycin-Sensitive 5′-Terminal Oligopyrimidine mRNA Translation and Reveal a Mitogen-Activated Protein Kinase-Dependent S6 Kinase Pathway , 2004, Molecular and Cellular Biology.
[51] T. Hewett,et al. Calcineurin A &bgr; Gene Targeting Predisposes the Myocardium to Acute Ischemia-Induced Apoptosis and Dysfunction , 2004, Circulation research.
[52] Jian Xu,et al. Calcineurin/NFAT Coupling Participates in Pathological, but not Physiological, Cardiac Hypertrophy , 2004, Circulation research.
[53] Y. Ahn,et al. Nuclear Targeting of Akt Enhances Kinase Activity and Survival of Cardiomyocytes , 2003, Circulation research.
[54] F. Mayer,et al. [Endurance training and cardial adaptation (athlete's heart)]. , 2004, Herz.
[55] E. Olson,et al. Balancing contractility and energy production: the role of myocyte enhancer factor 2 (MEF2) in cardiac hypertrophy. , 2004, Recent progress in hormone research.
[56] C. Kuan,et al. c‐Jun N‐terminal kinases (JNK) antagonize cardiac growth through cross‐talk with calcineurin–NFAT signaling , 2003, The EMBO journal.
[57] P. Kang,et al. Phosphoinositide 3-kinase(p110α) plays a critical role for the induction of physiological, but not pathological, cardiac hypertrophy , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[58] Michael D. Schneider,et al. Sizing up the heart: development redux in disease. , 2003, Genes & development.
[59] R. Liao,et al. Deletion of cytosolic phospholipase A2 promotes striated muscle growth , 2003, Nature Medicine.
[60] I. Komuro,et al. Roles of cardiac transcription factors in cardiac hypertrophy. , 2003, Circulation research.
[61] Timothy E Hewett,et al. Targeted inhibition of p38 MAPK promotes hypertrophic cardiomyopathy through upregulation of calcineurin-NFAT signaling. , 2003, The Journal of clinical investigation.
[62] S. Vatner,et al. Activation of Mst1 causes dilated cardiomyopathy by stimulating apoptosis without compensatory ventricular myocyte hypertrophy. , 2003, The Journal of clinical investigation.
[63] C. O'connor,et al. Pharmacologic therapy for patients with chronic heart failure and reduced systolic function: review of trials and practical considerations. , 2003, The American journal of cardiology.
[64] P. Doevendans,et al. Molecular determinants of myocardial hypertrophy and failure: alternative pathways for beneficial and maladaptive hypertrophy. , 2003, European heart journal.
[65] F. Dequiedt,et al. Class II histone deacetylases: versatile regulators. , 2003, Trends in genetics : TIG.
[66] Q. Liang,et al. Reengineering Inducible Cardiac-Specific Transgenesis With an Attenuated Myosin Heavy Chain Promoter , 2003, Circulation research.
[67] J. Molkentin,et al. Temporal activation of c‐Jun N‐terminal kinase in adult transgenic heart via cre‐loxP‐mediated DNA recombination , 2003, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[68] P. Kang,et al. Apoptosis in heart: basic mechanisms and implications in cardiovascular diseases. , 2003, Trends in molecular medicine.
[69] W. Manning,et al. Rapamycin Attenuates Load-Induced Cardiac Hypertrophy in Mice , 2003, Circulation.
[70] Attila Kovacs,et al. The role of the Grb2-p38 MAPK signaling pathway in cardiac hypertrophy and fibrosis. , 2003, The Journal of clinical investigation.
[71] A. V. van Kuilenburg,et al. Histone deacetylases (HDACs): characterization of the classical HDAC family. , 2003, The Biochemical journal.
[72] Carmen Birchmeier,et al. ErbB2 pathways in heart and neural diseases. , 2003, Trends in cardiovascular medicine.
[73] Rick B. Vega,et al. Dual roles of modulatory calcineurin-interacting protein 1 in cardiac hypertrophy , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[74] Luigi Fratta,et al. Melusin, a muscle-specific integrin β1–interacting protein, is required to prevent cardiac failure in response to chronic pressure overload , 2003, Nature Medicine.
[75] Masahiko Hoshijima,et al. The Cardiac Mechanical Stretch Sensor Machinery Involves a Z Disc Complex that Is Defective in a Subset of Human Dilated Cardiomyopathy , 2002, Cell.
[76] J. Molkentin,et al. Targeted Disruption of NFATc3, but Not NFATc4, Reveals an Intrinsic Defect in Calcineurin-Mediated Cardiac Hypertrophic Growth , 2002, Molecular and Cellular Biology.
[77] A. Giordano,et al. Activation and function of cyclin T–Cdk9 (positive transcription elongation factor-b) in cardiac muscle-cell hypertrophy , 2002, Nature Medicine.
[78] Daniel Levy,et al. Long-term trends in the incidence of and survival with heart failure. , 2002, The New England journal of medicine.
[79] J. Saffitz,et al. c-Jun N-Terminal Kinase Activation Mediates Downregulation of Connexin43 in Cardiomyocytes , 2002, Circulation research.
[80] C. Kahn,et al. Regulation of Myocardial Contractility and Cell Size by Distinct PI3K-PTEN Signaling Pathways , 2002, Cell.
[81] J. Ross,et al. Akt induces enhanced myocardial contractility and cell size in vivo in transgenic mice , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[82] Chun Li Zhang,et al. Class II Histone Deacetylases Act as Signal-Responsive Repressors of Cardiac Hypertrophy , 2002, Cell.
[83] H. Drexler,et al. Inhibition of calcineurin-NFAT hypertrophy signaling by cGMP-dependent protein kinase type I in cardiac myocytes , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[84] S. Cook,et al. Phenotypic Spectrum Caused by Transgenic Overexpression of Activated Akt in the Heart* , 2002, The Journal of Biological Chemistry.
[85] Carmen Birchmeier,et al. Conditional mutation of the ErbB2 (HER2) receptor in cardiomyocytes leads to dilated cardiomyopathy , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[86] J. Molkentin,et al. Divergent signaling pathways converge on GATA4 to regulate cardiac hypertrophic gene expression. , 2002, Journal of molecular and cellular cardiology.
[87] Lewis C Cantley,et al. The phosphoinositide 3-kinase pathway. , 2002, Science.
[88] Susumu Minamisawa,et al. ErbB2 is essential in the prevention of dilated cardiomyopathy , 2002, Nature Medicine.
[89] W. Kolch,et al. Extracellular signal regulated kinase (ERK)/mitogen activated protein kinase (MAPK)-independent functions of Raf kinases. , 2002, Journal of cell science.
[90] P. Kang,et al. Akt/Protein Kinase B Promotes Organ Growth in Transgenic Mice , 2002, Molecular and Cellular Biology.
[91] R. Weiss,et al. Targeted Inhibition of Calcineurin in Pressure-overload Cardiac Hypertrophy , 2002, The Journal of Biological Chemistry.
[92] J. Molkentin,et al. Impaired cardiac hypertrophic response in Calcineurin Aβ-deficient mice , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[93] S. Cherry,et al. Cardiac Myocyte-Specific Excision of the &bgr;1 Integrin Gene Results in Myocardial Fibrosis and Cardiac Failure , 2002, Circulation research.
[94] P. Doevendans,et al. Calcineurin and hypertrophic heart disease: novel insights and remaining questions. , 2002, Cardiovascular research.
[95] Robert J. Lefkowitz,et al. Seven-transmembrane-spanning receptors and heart function , 2002, Nature.
[96] E. Olson,et al. Activated glycogen synthase-3β suppresses cardiac hypertrophy in vivo , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[97] C. Trautwein,et al. Gene Transfer of cGMP-Dependent Protein Kinase I Enhances the Antihypertrophic Effects of Nitric Oxide in Cardiomyocytes , 2002, Hypertension.
[98] R. Ross,et al. Integrins and the myocardium. , 2001, Genetic engineering.
[99] Hiroshi Asanuma,et al. Cardiac hypertrophy is inhibited by antagonism of ADAM12 processing of HB-EGF: Metalloproteinase inhibitors as a new therapy , 2002, Nature Medicine.
[100] W. Koch,et al. Genetic Alterations That Inhibit In Vivo Pressure-Overload Hypertrophy Prevent Cardiac Dysfunction Despite Increased Wall Stress , 2002, Circulation.
[101] K. Chien,et al. Absence of pressure overload induced myocardial hypertrophy after conditional inactivation of Gαq/Gα11 in cardiomyocytes , 2001, Nature Medicine.
[102] M. Birnbaum,et al. Akt1/PKBα Is Required for Normal Growth but Dispensable for Maintenance of Glucose Homeostasis in Mice* , 2001, The Journal of Biological Chemistry.
[103] D. Kass,et al. The in vivo role of p38 MAP kinases in cardiac remodeling and restrictive cardiomyopathy , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[104] I. Roninson,et al. Growth retardation and increased apoptosis in mice with homozygous disruption of the Akt1 gene. , 2001, Genes & development.
[105] J. Molkentin,et al. The Transcription Factors GATA4 and GATA6 Regulate Cardiomyocyte Hypertrophy in Vitro and in Vivo * , 2001, The Journal of Biological Chemistry.
[106] C. Allis,et al. Translating the Histone Code , 2001, Science.
[107] S. Kudoh,et al. Calcineurin Plays a Critical Role in the Development of Pressure Overload–Induced Cardiac Hypertrophy , 2001, Circulation.
[108] K. Kaestner,et al. Insulin Resistance and a Diabetes Mellitus-Like Syndrome in Mice Lacking the Protein Kinase Akt2 (PKBβ) , 2001 .
[109] E. Olson,et al. Activated MEK5 induces serial assembly of sarcomeres and eccentric cardiac hypertrophy , 2001, The EMBO journal.
[110] K. Khrapko,et al. Cardiomyopathy in transgenic mice with cardiac-specific overexpression of serum response factor. , 2001, American journal of physiology. Heart and circulatory physiology.
[111] A. Ullrich,et al. Cell communication networks: epidermal growth factor receptor transactivation as the paradigm for interreceptor signal transmission , 2001, Oncogene.
[112] Rick B. Vega,et al. Myocyte-enriched calcineurin-interacting protein, MCIP1, inhibits cardiac hypertrophy in vivo , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[113] R. Hajjar,et al. Targeted inhibition of calcineurin attenuates cardiac hypertrophy in vivo , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[114] G. Dorn,et al. Cytoplasmic signaling pathways that regulate cardiac hypertrophy. , 2001, Annual review of physiology.
[115] E. Olson,et al. Calsarcins, a novel family of sarcomeric calcineurin-binding proteins. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[116] J. Molkentin. The Zinc Finger-containing Transcription Factors GATA-4, -5, and -6 , 2000, The Journal of Biological Chemistry.
[117] R. Kitsis,et al. The MEK1–ERK1/2 signaling pathway promotes compensated cardiac hypertrophy in transgenic mice , 2000, The EMBO journal.
[118] P. Kang,et al. The conserved phosphoinositide 3‐kinase pathway determines heart size in mice , 2000, The EMBO journal.
[119] R. Passier,et al. CaM kinase signaling induces cardiac hypertrophy and activates the MEF2 transcription factor in vivo. , 2000, The Journal of clinical investigation.
[120] Paul A. Overbeek,et al. TAK1 is activated in the myocardium after pressure overload and is sufficient to provoke heart failure in transgenic mice , 2000, Nature Medicine.
[121] E. Olson,et al. Signal-dependent activation of the MEF2 transcription factor by dissociation from histone deacetylases. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[122] W. Kannel,et al. Vital epidemiologic clues in heart failure. , 2000, Journal of clinical epidemiology.
[123] J. Molkentin,et al. Regulation of MEF2 by p38 MAPK and its implication in cardiomyocyte biology. , 2000, Trends in cardiovascular medicine.
[124] M. Malek. Health economics of heart failure , 1999, Heart.
[125] E. Hafen,et al. Drosophila S6 kinase: a regulator of cell size. , 1999, Science.
[126] Michael Karin,et al. The Beginning of the End: IκB Kinase (IKK) and NF-κB Activation* , 1999, The Journal of Biological Chemistry.
[127] E. Miska,et al. MEF‐2 function is modified by a novel co‐repressor, MITR , 1999, The EMBO journal.
[128] E. Miska,et al. HDAC4 deacetylase associates with and represses the MEF2 transcription factor , 1999, The EMBO journal.
[129] Anthony J. Muslin,et al. RGS4 causes increased mortality and reduced cardiac hypertrophy in response to pressure overload. , 1999, The Journal of clinical investigation.
[130] A. Clerk,et al. Activation of protein kinase cascades in the heart by hypertrophic G protein-coupled receptor agonists. , 1999, The American journal of cardiology.
[131] G L Johnson,et al. Organization and regulation of mitogen-activated protein kinase signaling pathways. , 1999, Current opinion in cell biology.
[132] F. Zannad,et al. Incidence, clinical and etiologic features, and outcomes of advanced chronic heart failure: the EPICAL Study. Epidémiologie de l'Insuffisance Cardiaque Avancée en Lorraine. , 1999, Journal of the American College of Cardiology.
[133] J. Croft,et al. Hospitalization of patients with heart failure: National Hospital Discharge Survey, 1985 to 1995. , 1999, American heart journal.
[134] Stefano Fumagalli,et al. Disruption of the p70s6k/p85s6k gene reveals a small mouse phenotype and a new functional S6 kinase , 1998, The EMBO journal.
[135] E. Neer,et al. Transient cardiac expression of constitutively active Galphaq leads to hypertrophy and dilated cardiomyopathy by calcineurin-dependent and independent pathways. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[136] D. Levy,et al. Increased left ventricular mass and hypertrophy are associated with increased risk for sudden death. , 1998, Journal of the American College of Cardiology.
[137] A. Clerk,et al. "Stress-responsive" mitogen-activated protein kinases (c-Jun N-terminal kinases and p38 mitogen-activated protein kinases) in the myocardium. , 1998, Circulation research.
[138] John W. Adams,et al. Enhanced Galphaq signaling: a common pathway mediates cardiac hypertrophy and apoptotic heart failure. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[139] R. Lefkowitz,et al. Targeting the receptor-Gq interface to inhibit in vivo pressure overload myocardial hypertrophy. , 1998, Science.
[140] Jeffrey Robbins,et al. A Calcineurin-Dependent Transcriptional Pathway for Cardiac Hypertrophy , 1998, Cell.
[141] G. Dorn,et al. Transgenic Gαq overexpression induces cardiac contractile failure in mice , 1997 .
[142] Minoru Hongo,et al. MLP-Deficient Mice Exhibit a Disruption of Cardiac Cytoarchitectural Organization, Dilated Cardiomyopathy, and Heart Failure , 1997, Cell.
[143] K. Chien,et al. Ventricular Expression of a MLC-2v-ras Fusion Gene Induces Cardiac Hypertrophy and Selective Diastolic Dysfunction in Transgenic Mice (*) , 1995, The Journal of Biological Chemistry.