Literature DB >> 12524460

Cardiac hypertrophy: the good, the bad, and the ugly.

N Frey1, E N Olson.   

Abstract

Cardiac hypertrophy is the heart's response to a variety of extrinsic and intrinsic stimuli that impose increased biomechanical stress. While hypertrophy can eventually normalize wall tension, it is associated with an unfavorable outcome and threatens affected patients with sudden death or progression to overt heart failure. Accumulating evidence from studies in human patients and animal models suggests that in most instances hypertrophy is not a compensatory response to the change in mechanical load, but rather is a maladaptive process. Accordingly, modulation of myocardial growth without adversely affecting contractile function is increasingly recognized as a potentially auspicious approach in the prevention and treatment of heart failure. In this review, we summarize recent insights into hypertrophic signaling and consider several novel antihypertrophic strategies.

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Year:  2003        PMID: 12524460     DOI: 10.1146/annurev.physiol.65.092101.142243

Source DB:  PubMed          Journal:  Annu Rev Physiol        ISSN: 0066-4278            Impact factor:   19.318


  482 in total

1.  Thyroid hormone inhibits ERK phosphorylation in pressure overload-induced hypertrophied mouse hearts through a receptor-mediated mechanism.

Authors:  Jorge Suarez; Brian T Scott; Jorge A Suarez-Ramirez; Citlalic V Chavira; Wolfgang H Dillmann
Journal:  Am J Physiol Cell Physiol       Date:  2010-10-06       Impact factor: 4.249

2.  The direct incorporation of perfusion defect information to define ischemia and infarction in a finite element model of the left ventricle.

Authors:  Alexander I Veress; George S K Fung; Taek-Soo Lee; Benjamin M W Tsui; Gregory A Kicska; W Paul Segars; Grant T Gullberg
Journal:  J Biomech Eng       Date:  2015-02-25       Impact factor: 2.097

3.  Calcium-mediated histone modifications regulate alternative splicing in cardiomyocytes.

Authors:  Alok Sharma; Hieu Nguyen; Cuiyu Geng; Melissa N Hinman; Guangbin Luo; Hua Lou
Journal:  Proc Natl Acad Sci U S A       Date:  2014-11-03       Impact factor: 11.205

Review 4.  Advances in exploring the role of microRNAs in the pathogenesis, diagnosis and therapy of cardiac diseases in China.

Authors:  Z W Pan; Y J Lu; B F Yang
Journal:  Br J Pharmacol       Date:  2015-01-20       Impact factor: 8.739

Review 5.  Cardiac hypertrophy and heart failure development through Gq and CaM kinase II signaling.

Authors:  Shikha Mishra; Haiyun Ling; Michael Grimm; Tong Zhang; Don M Bers; Joan Heller Brown
Journal:  J Cardiovasc Pharmacol       Date:  2010-12       Impact factor: 3.105

Review 6.  A-kinase anchoring proteins that regulate cardiac remodeling.

Authors:  Graeme K Carnegie; Brian T Burmeister
Journal:  J Cardiovasc Pharmacol       Date:  2011-11       Impact factor: 3.105

Review 7.  Pseudophosphorylation of cardiac myosin regulatory light chain: a promising new tool for treatment of cardiomyopathy.

Authors:  Sunil Yadav; Danuta Szczesna-Cordary
Journal:  Biophys Rev       Date:  2017-01-25

8.  Short-term akt activation in cardiac muscle cells improves contractile function in failing hearts.

Authors:  Ichiro Shiojima; Stephan Schiekofer; Jochen G Schneider; Kurt Belisle; Kaori Sato; Martin Andrassy; Gennaro Galasso; Kenneth Walsh
Journal:  Am J Pathol       Date:  2012-09-30       Impact factor: 4.307

9.  The delta isoform of CaM kinase II is required for pathological cardiac hypertrophy and remodeling after pressure overload.

Authors:  Johannes Backs; Thea Backs; Stefan Neef; Michael M Kreusser; Lorenz H Lehmann; David M Patrick; Chad E Grueter; Xiaoxia Qi; James A Richardson; Joseph A Hill; Hugo A Katus; Rhonda Bassel-Duby; Lars S Maier; Eric N Olson
Journal:  Proc Natl Acad Sci U S A       Date:  2009-01-28       Impact factor: 11.205

10.  The CRM1 nuclear export receptor controls pathological cardiac gene expression.

Authors:  Brooke C Harrison; Charles R Roberts; David B Hood; Meghan Sweeney; Jody M Gould; Erik W Bush; Timothy A McKinsey
Journal:  Mol Cell Biol       Date:  2004-12       Impact factor: 4.272

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