Literature DB >> 12900219

The molecular basis of myocardial hypertrophy and heart failure.

Oliver Ritter1, Ludwig Neyses.   

Abstract

Heart failure (HF) is the inability of the heart to cope with the metabolic demands of the periphery. It is the common end-stage of many frequent cardiac diseases and is characterized by relentless progression. Mechanisms of progression include renal sodium and water retention, neurohumoral activation and alterations of the protein composition (gene programme) of the heart itself. In this review, we explain the often confusing terminology in the subject, briefly touch upon the peripheral mechanisms of HF, and then focus on the changes in the gene programme of the failing heart and the molecular mechanisms leading to them. Understanding the basic processes underlying HF will help uninitiated readers to gain insight into recent novel approaches to its treatment.

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Year:  2003        PMID: 12900219     DOI: 10.1016/s1471-4914(03)00114-x

Source DB:  PubMed          Journal:  Trends Mol Med        ISSN: 1471-4914            Impact factor:   11.951


  14 in total

1.  Enhanced hypertrophy in ob/ob mice due to an impairment in expression of atrial natriuretic peptide.

Authors:  Eduardo Mascareno; Daniel Beckles; Manya Dhar-Mascareno; M A Q Siddiqui
Journal:  Vascul Pharmacol       Date:  2009-06-26       Impact factor: 5.773

2.  PAR1-dependent COX-2/PGE2 production contributes to cell proliferation via EP2 receptors in primary human cardiomyocytes.

Authors:  Peter Tzu-Yu Chien; Hsi-Lung Hsieh; Pei-Ling Chi; Chuen-Mao Yang
Journal:  Br J Pharmacol       Date:  2014-09-05       Impact factor: 8.739

3.  Increase in cardiac myosin heavy-chain (MyHC) alpha protein isoform in hibernating ground squirrels, with echocardiographic visualization of ventricular wall hypertrophy and prolonged contraction.

Authors:  O Lynne Nelson; Bryan C Rourke
Journal:  J Exp Biol       Date:  2013-09-26       Impact factor: 3.312

Review 4.  The role of TWEAK/Fn14 in cardiac remodeling.

Authors:  Man-Yi Ren; Shu-Jian Sui
Journal:  Mol Biol Rep       Date:  2012-06-30       Impact factor: 2.316

5.  ANGPTL8 is a negative regulator in pathological cardiac hypertrophy.

Authors:  Lin Hu; Jiarui Wei; Yue Zhang; Ziyuan Wang; Junming Tang; Jian Tang; Yujiu Gao; Xiaoqiao Zhang; Yifan Li; Yantong Liu; Shinan Ma; Xingrong Guo; Qiufang Zhang
Journal:  Cell Death Dis       Date:  2022-07-18       Impact factor: 9.685

6.  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

7.  SERCA inhibition limits the functional effects of cyclic GMP in both control and hypertrophic cardiac myocytes.

Authors:  Qihang Zhang; Tomer Davidov; Harvey R Weiss; Peter M Scholz
Journal:  Pharmacology       Date:  2009-03-04       Impact factor: 2.547

8.  Cardiomyocyte-GSK-3α promotes mPTP opening and heart failure in mice with chronic pressure overload.

Authors:  Firdos Ahmad; Anand P Singh; Dhanendra Tomar; Mohamed Rahmani; Qinkun Zhang; James R Woodgett; Douglas G Tilley; Hind Lal; Thomas Force
Journal:  J Mol Cell Cardiol       Date:  2019-03-27       Impact factor: 5.000

9.  Developmental and lifelong dioxin exposure induces measurable changes in cardiac structure and function in adulthood.

Authors:  Matthew de Gannes; Sheryl E Koch; Alvaro Puga; Jack Rubinstein
Journal:  Sci Rep       Date:  2021-05-17       Impact factor: 4.379

10.  GJA1-20k attenuates Ang II-induced pathological cardiac hypertrophy by regulating gap junction formation and mitochondrial function.

Authors:  Yi-le Fu; Liang Tao; Fu-Hua Peng; Ning-Ze Zheng; Qing Lin; Shao-Yi Cai; Qin Wang
Journal:  Acta Pharmacol Sin       Date:  2020-07-03       Impact factor: 6.150

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