Literature DB >> 10377279

Cardiac hypertrophy: sorting out the circuitry.

T A McKinsey1, E N Olson.   

Abstract

Cardiac hypertrophy is an adaptive response of the heart to a variety of intrinsic and extrinsic stimuli. The hypertrophic response, during which cardiomyocytes increase in size without undergoing cell division, initially serves to compensate for decreased cardiac output; however, prolonged hypertrophy can become detrimental, resulting in dilated cardiomyopathy and heart failure. Cardiac hypertrophy requires coupling of intracellular signal transduction systems with transcription factors that activate and maintain the hypertrophic program. Over the past year, signaling pathways involving G proteins, mitogen-activated protein kinases and calcium-responsive phosphatases have emerged as critical regulators of cardiac hypertrophy.

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Year:  1999        PMID: 10377279     DOI: 10.1016/s0959-437x(99)80040-9

Source DB:  PubMed          Journal:  Curr Opin Genet Dev        ISSN: 0959-437X            Impact factor:   5.578


  27 in total

Review 1.  Transcriptional mechanisms regulating Ca(2+) homeostasis.

Authors:  Michael F Ritchie; Yandong Zhou; Jonathan Soboloff
Journal:  Cell Calcium       Date:  2010-11-13       Impact factor: 6.817

Review 2.  Electrical and mechanical stimulation of cardiac cells and tissue constructs.

Authors:  Whitney L Stoppel; David L Kaplan; Lauren D Black
Journal:  Adv Drug Deliv Rev       Date:  2015-07-30       Impact factor: 15.470

3.  Suppressor of cytokine signaling-3 is a biomechanical stress-inducible gene that suppresses gp130-mediated cardiac myocyte hypertrophy and survival pathways.

Authors:  H Yasukawa; M Hoshijima; Y Gu; T Nakamura; S Pradervand; T Hanada; Y Hanakawa; A Yoshimura; J Ross; K R Chien
Journal:  J Clin Invest       Date:  2001-11       Impact factor: 14.808

4.  Signal-dependent activation of the MEF2 transcription factor by dissociation from histone deacetylases.

Authors:  J Lu; T A McKinsey; R L Nicol; E N Olson
Journal:  Proc Natl Acad Sci U S A       Date:  2000-04-11       Impact factor: 11.205

5.  Dilated cardiomyopathy and impaired cardiac hypertrophic response to angiotensin II in mice lacking FGF-2.

Authors:  C Pellieux; A Foletti; G Peduto; J F Aubert; J Nussberger; F Beermann; H R Brunner; T Pedrazzini
Journal:  J Clin Invest       Date:  2001-12       Impact factor: 14.808

Review 6.  Mitogen-activated protein kinase inhibitor regulation of heart function and fibrosis in cardiomyopathy caused by lamin A/C gene mutation.

Authors:  Antoine Muchir; Wei Wu; Howard J Worman
Journal:  Trends Cardiovasc Med       Date:  2010-10       Impact factor: 6.677

7.  Cardiac hypertrophy and histone deacetylase-dependent transcriptional repression mediated by the atypical homeodomain protein Hop.

Authors:  Hyun Kook; John J Lepore; Aaron D Gitler; Min Min Lu; Wendy Wing-Man Yung; Joel Mackay; Rong Zhou; Victor Ferrari; Peter Gruber; Jonathan A Epstein
Journal:  J Clin Invest       Date:  2003-09       Impact factor: 14.808

8.  Positive transcription elongation factor b activity in compensatory myocardial hypertrophy is regulated by cardiac lineage protein-1.

Authors:  Jorge Espinoza-Derout; Michael Wagner; Louis Salciccioli; Jason M Lazar; Sikha Bhaduri; Eduardo Mascareno; Brahim Chaqour; M A Q Siddiqui
Journal:  Circ Res       Date:  2009-05-14       Impact factor: 17.367

Review 9.  Roles of TRP channels in the development of cardiac hypertrophy.

Authors:  Motohiro Nishida; Hitoshi Kurose
Journal:  Naunyn Schmiedebergs Arch Pharmacol       Date:  2008-07-04       Impact factor: 3.000

10.  TEF-1 and C/EBPbeta are major p38alpha MAPK-regulated transcription factors in proliferating cardiomyocytes.

Authors:  Concetta Ambrosino; Tomoko Iwata; Claudio Scafoglio; Massimo Mallardo; Rüdiger Klein; Angel R Nebreda
Journal:  Biochem J       Date:  2006-05-15       Impact factor: 3.857

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