Literature DB >> 16138008

Cardiomyocyte proliferation: a platform for mammalian cardiac repair.

Felix B Engel1.   

Abstract

Permanent loss of heart muscle cells, cardiomyocytes, is a major mechanism resulting in ventricular dysfunction and heart failure. Potential solutions to this problem could be either to stimulate the heart to generate new cells by inducing existing cardiomyocytes to divide or to activate or deliver stem cells/ progenitor cells to multiply and subsequently differentiate into cardiomyocytes. Utilizing in vitro and in vivo approaches, p38 MAP kinase has recently been identified as a key negative regulator of cardiomyocyte proliferation. This work provides strong evidence that adult mammalian cardiomyocytes can divide. This review discusses the potential of the induction of mammalian cardiomyocyte proliferation as a therapeutic strategy for myocardial repair.

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Year:  2005        PMID: 16138008     DOI: 10.4161/cc.4.10.2081

Source DB:  PubMed          Journal:  Cell Cycle        ISSN: 1551-4005            Impact factor:   4.534


  24 in total

1.  Specific regulation of noncanonical p38alpha activation by Hsp90-Cdc37 chaperone complex in cardiomyocyte.

Authors:  Asuka Ota; Jun Zhang; Peipei Ping; Jiahuai Han; Yibin Wang
Journal:  Circ Res       Date:  2010-03-18       Impact factor: 17.367

Review 2.  Mitogen-activated protein kinases in heart development and diseases.

Authors:  Yibin Wang
Journal:  Circulation       Date:  2007-09-18       Impact factor: 29.690

3.  Knockdown of cyclin-dependent kinase inhibitors induces cardiomyocyte re-entry in the cell cycle.

Authors:  Valeria Di Stefano; Mauro Giacca; Maurizio C Capogrossi; Marco Crescenzi; Fabio Martelli
Journal:  J Biol Chem       Date:  2011-01-05       Impact factor: 5.157

Review 4.  Cardiomyocyte maturation: advances in knowledge and implications for regenerative medicine.

Authors:  Elaheh Karbassi; Aidan Fenix; Silvia Marchiano; Naoto Muraoka; Kenta Nakamura; Xiulan Yang; Charles E Murry
Journal:  Nat Rev Cardiol       Date:  2020-02-03       Impact factor: 32.419

5.  Degradation of p21Cip1 through anaphase-promoting complex/cyclosome and its activator Cdc20 (APC/CCdc20) ubiquitin ligase complex-mediated ubiquitylation is inhibited by cyclin-dependent kinase 2 in cardiomyocytes.

Authors:  Kazuhiko Yamada; Mimi Tamamori-Adachi; Ikuko Goto; Masayoshi Iizuka; Takashi Yasukawa; Teijiro Aso; Tomoki Okazaki; Shigetaka Kitajima
Journal:  J Biol Chem       Date:  2011-11-01       Impact factor: 5.157

6.  Temporal evaluation of cardiac myocyte hypertrophy and hyperplasia in male rats secondary to chronic volume overload.

Authors:  Yan Du; Eric Plante; Joseph S Janicki; Gregory L Brower
Journal:  Am J Pathol       Date:  2010-07-22       Impact factor: 4.307

7.  MAPK-activated protein kinase-2 in cardiac hypertrophy and cyclooxygenase-2 regulation in heart.

Authors:  John M Streicher; Shuxun Ren; Harvey Herschman; Yibin Wang
Journal:  Circ Res       Date:  2010-03-25       Impact factor: 17.367

8.  Sulfaphenazole protects heart against ischemia-reperfusion injury and cardiac dysfunction by overexpression of iNOS, leading to enhancement of nitric oxide bioavailability and tissue oxygenation.

Authors:  Mahmood Khan; Iyyapu K Mohan; Vijay K Kutala; Sainath R Kotha; Narasimham L Parinandi; Robert L Hamlin; Periannan Kuppusamy
Journal:  Antioxid Redox Signal       Date:  2009-04       Impact factor: 8.401

9.  A-kinase anchoring protein Lbc coordinates a p38 activating signaling complex controlling compensatory cardiac hypertrophy.

Authors:  Irene Pérez López; Luca Cariolato; Darko Maric; Ludovic Gillet; Hugues Abriel; Dario Diviani
Journal:  Mol Cell Biol       Date:  2013-05-28       Impact factor: 4.272

10.  Combining neuropeptide Y and mesenchymal stem cells reverses remodeling after myocardial infarction.

Authors:  Yigang Wang; Dongsheng Zhang; Muhammad Ashraf; Tiemin Zhao; Wei Huang; Atif Ashraf; Ambikaipakan Balasubramaniam
Journal:  Am J Physiol Heart Circ Physiol       Date:  2009-11-06       Impact factor: 4.733

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