Literature DB >> 12890171

Cardiac hypertrophy: a matter of translation.

R D Hannan1, A Jenkins, A K Jenkins, Y Brandenburger.   

Abstract

1. Left ventricular hypertrophy (LVH) of the heart is an adaptive response to sustained increases in blood pressure and hormone imbalances. Left ventricular hypertrophy is associated with programmed responses at the molecular and biochemical level in different subsets of cardiac cells, including the cardiac muscle cells (cardiomyocytes), fibroblasts, conductive tissue and coronary vasculature. 2. Regardless of the initiating cause, the actual increase in chamber enlargement is, in each case, due to an increase in size of a pre-existing cardiomyocyte population, with little or no change in their number; a process referred to as cellular hypertrophy. 3. An accelerated rate of global protein synthesis is the primary mechanism by which protein accumulation increases during cardiomyocyte hypertrophy. In turn, increased rates of synthesis are a result of increased translational rates of existing ribosomes (translational efficiency) and/or synthesis and recruitment of additional ribosomes (translational capacity). 4. The present review examines the relative importance of translational capacity and translational efficiency in the response of myocytes to acute and chronic demands for increased protein synthesis and the role of these mechanisms in the development of LVH.

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Year:  2003        PMID: 12890171     DOI: 10.1046/j.1440-1681.2003.03873.x

Source DB:  PubMed          Journal:  Clin Exp Pharmacol Physiol        ISSN: 0305-1870            Impact factor:   2.557


  54 in total

1.  Resveratrol prevents pathological but not physiological cardiac hypertrophy.

Authors:  Vernon W Dolinsky; Carrie-Lynn M Soltys; Kyle J Rogan; Anita Y M Chan; Jeevan Nagendran; Shaohua Wang; Jason R B Dyck
Journal:  J Mol Med (Berl)       Date:  2014-11-15       Impact factor: 4.599

2.  Novel 5'TOPmRNAs regulated by ribosomal S6 kinase are important for cardiomyocyte development: S6 kinase suppression limits cardiac differentiation and promotes pluripotent cells toward a neural lineage.

Authors:  LeeAnn Li; Shannon M Larabee; Shenglin Chen; Ladan Basiri; Seiji Yamaguchi; Asif Zakaria; G Ian Gallicano
Journal:  Stem Cells Dev       Date:  2012-02-08       Impact factor: 3.272

3.  UAP56 is an important regulator of protein synthesis and growth in cardiomyocytes.

Authors:  Abha Sahni; Nadan Wang; Jeffrey D Alexis
Journal:  Biochem Biophys Res Commun       Date:  2010-01-29       Impact factor: 3.575

4.  IGF-I activates the eIF4F system in cardiac muscle in vivo.

Authors:  Thomas C Vary; Charles H Lang
Journal:  Mol Cell Biochem       Date:  2005-04       Impact factor: 3.396

5.  Homeostatic regulation of electrical excitability in physiological cardiac hypertrophy.

Authors:  Kai-Chien Yang; Nicholas C Foeger; Céline Marionneau; Patrick Y Jay; Julie R McMullen; Jeanne M Nerbonne
Journal:  J Physiol       Date:  2010-10-25       Impact factor: 5.182

6.  Interrogating translational efficiency and lineage-specific transcriptomes using ribosome affinity purification.

Authors:  Pingzhu Zhou; Yijing Zhang; Qing Ma; Fei Gu; Daniel S Day; Aibin He; Bin Zhou; Jing Li; Sean M Stevens; Daniel Romo; William T Pu
Journal:  Proc Natl Acad Sci U S A       Date:  2013-09-03       Impact factor: 11.205

Review 7.  Adaptive mechanisms to compensate for overnutrition-induced cardiovascular abnormalities.

Authors:  Lakshmi Pulakat; Vincent G DeMarco; Sivakumar Ardhanari; Anand Chockalingam; Rukhsana Gul; Adam Whaley-Connell; James R Sowers
Journal:  Am J Physiol Regul Integr Comp Physiol       Date:  2011-08-03       Impact factor: 3.619

8.  Activation of protein synthesis in cardiomyocytes by the hypertrophic agent phenylephrine requires the activation of ERK and involves phosphorylation of tuberous sclerosis complex 2 (TSC2).

Authors:  Mark Rolfe; Laura E McLeod; Phillip F Pratt; Christopher G Proud
Journal:  Biochem J       Date:  2005-06-15       Impact factor: 3.857

9.  Distinct cellular and molecular mechanisms underlie functional remodeling of repolarizing K+ currents with left ventricular hypertrophy.

Authors:  Céline Marionneau; Sylvain Brunet; Thomas P Flagg; Thomas K Pilgram; Sophie Demolombe; Jeanne M Nerbonne
Journal:  Circ Res       Date:  2008-05-01       Impact factor: 17.367

10.  Cardiac deletion of Smyd2 is dispensable for mouse heart development.

Authors:  Florian Diehl; Mark A Brown; Machteld J van Amerongen; Tatyana Novoyatleva; Astrid Wietelmann; June Harriss; Fulvia Ferrazzi; Thomas Böttger; Richard P Harvey; Philip W Tucker; Felix B Engel
Journal:  PLoS One       Date:  2010-03-17       Impact factor: 3.240

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