Literature DB >> 21239247

Control of cardiac muscle cell division.

W C Claycomb1.   

Abstract

Division and proliferation of the terminally differentiated ventricular heart muscle cell in the adult mammal is not activated after injury such as that caused by a myocardial infarction. We do not understand how mitosis is irreversibly blocked in these myocytes during early development. Mammalian cardiac muscle, unlike skeletal muscle, cannot regenerate. Knowledge of the mechanisms that control the cardiac myocyte cell cycle would allow us to design reagents or procedures to initiate repair or regeneration of the adult myocardium following injury. Ideally, we would like to be able to revert cardiac muscle cells in intact heart muscle to the biochemical state they were in during early fetal growth when they were actively dividing and proliferating. This article briefly reviews what is currently known about the mechanism which so tightly suppresses the mitotic activity of these highly differentiated cells.
Copyright © 1992. Published by Elsevier Inc.

Entities:  

Year:  1992        PMID: 21239247     DOI: 10.1016/1050-1738(92)90030-V

Source DB:  PubMed          Journal:  Trends Cardiovasc Med        ISSN: 1050-1738            Impact factor:   6.677


  12 in total

1.  The MRE11-NBS1-RAD50 pathway is perturbed in SV40 large T antigen-immortalized AT-1, AT-2 and HL-1 cardiomyocytes.

Authors:  N A Lanson; D B Egeland; B A Royals; W C Claycomb
Journal:  Nucleic Acids Res       Date:  2000-08-01       Impact factor: 16.971

2.  Adult rat cardiomyocyte proliferation assay.

Authors:  D M Smith; W C Claycomb
Journal:  In Vitro Cell Dev Biol Anim       Date:  1997-06       Impact factor: 2.416

3.  Physiological contractility of cardiomyocytes in the wall of mouse and rat azygos vein.

Authors:  Rong Liu; Han-Zhong Feng; J-P Jin
Journal:  Am J Physiol Cell Physiol       Date:  2014-01-29       Impact factor: 4.249

4.  Embryonic stem cell-derived cardiomyocytes harbor a subpopulation of niche-forming Sca-1+ progenitor cells.

Authors:  May L Lam; Sherin I Hashem; William C Claycomb
Journal:  Mol Cell Biochem       Date:  2010-12-03       Impact factor: 3.396

5.  Transformation of adult ventricular myocytes with the temperature sensitive A58 (tsA58) mutant of the SV40 large T antigen.

Authors:  C Miller; J Rulfs; S R Jaspers; M Buckholt; T B Miller
Journal:  Mol Cell Biochem       Date:  1994-07-13       Impact factor: 3.396

6.  Cell-cycle dependent anti-FGF-2 staining of chicken cardiac myocytes: movement from chromosomal to cleavage furrow- and midbody-associated sites.

Authors:  L Liu; J Dai; R R Fandrich; E Kardami
Journal:  Mol Cell Biochem       Date:  1997-11       Impact factor: 3.396

Review 7.  Vitamin D deficiency in early life and the potential programming of cardiovascular disease in adulthood.

Authors:  Oksan Gezmish; Mary Jane Black
Journal:  J Cardiovasc Transl Res       Date:  2013-05-30       Impact factor: 4.132

8.  Increased cardiac workload by closure of the ductus arteriosus leads to hypertrophy and apoptosis rather than to hyperplasia in the late fetal period.

Authors:  Maurice J B van den Hoff; Ronald H Lekanne Deprez; Jan M Ruijter; Piet A J de Boer; Sabina Tesink-Taekema; Anita A Buffing; Wouter H Lamers; Antoon F M Moorman
Journal:  Naunyn Schmiedebergs Arch Pharmacol       Date:  2004-08-31       Impact factor: 3.000

9.  Discontinuous thoracic venous cardiomyocytes and heart exhibit synchronized developmental switch of troponin isoforms.

Authors:  Martin P Kracklauer; Han-Zhong Feng; Wenrui Jiang; Jenny L-C Lin; Jim J-C Lin; Jian-Ping Jin
Journal:  FEBS J       Date:  2013-01-02       Impact factor: 5.542

10.  Cardiac insulin-like growth factor-1 and cyclins gene expression in canine models of ischemic or overpacing cardiomyopathy.

Authors:  Maryam Mahmoudabady; Myrielle Mathieu; Karim Touihri; Ielham Hadad; Agnes Mendes Da Costa; Robert Naeije; Kathleen Mc Entee
Journal:  BMC Cardiovasc Disord       Date:  2009-10-09       Impact factor: 2.298

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