Cell cycle regulation to repair the infarcted myocardium

Joshua D. Dowell, Loren Field, Kishore B S Pasumarthi

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Lower vertebrates such as newt and zebrafish are able to reactivate high levels of cardiomyocyte cell cycle activity in response to experimental injury resulting in apparent regeneration. In contrast, damaged myocardium is replaced by fibrotic scar tissue in higher vertebrates. This process compromises the contractile function of the surviving myocardium, ultimately leading to heart failure. Various strategies are being pursued to augment myocyte number in the diseased hearts. One approach entails the reactivation of cell cycle in surviving cardiomyocytes. Here, we provide a summary of methods to monitor cell cycle activity, and interventions demonstrating positive cell cycle effects in cardiomyocytes as well as discuss the potential utility of cell cycle regulation to augment myocyte number in diseased hearts.

Original languageEnglish
Pages (from-to)293-303
Number of pages11
JournalHeart Failure Reviews
Volume8
Issue number3
DOIs
StatePublished - Jul 2003

Fingerprint

Myocardium
Cell Cycle
Cardiac Myocytes
Muscle Cells
Vertebrates
Heart Diseases
Salamandridae
Zebrafish
Cicatrix
Regeneration
Heart Failure
Wounds and Injuries

Keywords

  • Cardiomyocyte
  • Cell cycle
  • Myocardial repair

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Cell cycle regulation to repair the infarcted myocardium. / Dowell, Joshua D.; Field, Loren; Pasumarthi, Kishore B S.

In: Heart Failure Reviews, Vol. 8, No. 3, 07.2003, p. 293-303.

Research output: Contribution to journalArticle

Dowell, Joshua D. ; Field, Loren ; Pasumarthi, Kishore B S. / Cell cycle regulation to repair the infarcted myocardium. In: Heart Failure Reviews. 2003 ; Vol. 8, No. 3. pp. 293-303.
@article{05ac966e5ffb4f73b594a9d64f307ca2,
title = "Cell cycle regulation to repair the infarcted myocardium",
abstract = "Lower vertebrates such as newt and zebrafish are able to reactivate high levels of cardiomyocyte cell cycle activity in response to experimental injury resulting in apparent regeneration. In contrast, damaged myocardium is replaced by fibrotic scar tissue in higher vertebrates. This process compromises the contractile function of the surviving myocardium, ultimately leading to heart failure. Various strategies are being pursued to augment myocyte number in the diseased hearts. One approach entails the reactivation of cell cycle in surviving cardiomyocytes. Here, we provide a summary of methods to monitor cell cycle activity, and interventions demonstrating positive cell cycle effects in cardiomyocytes as well as discuss the potential utility of cell cycle regulation to augment myocyte number in diseased hearts.",
keywords = "Cardiomyocyte, Cell cycle, Myocardial repair",
author = "Dowell, {Joshua D.} and Loren Field and Pasumarthi, {Kishore B S}",
year = "2003",
month = "7",
doi = "10.1023/A:1024738104722",
language = "English",
volume = "8",
pages = "293--303",
journal = "Heart Failure Reviews",
issn = "1382-4147",
publisher = "Springer Netherlands",
number = "3",

}

TY - JOUR

T1 - Cell cycle regulation to repair the infarcted myocardium

AU - Dowell, Joshua D.

AU - Field, Loren

AU - Pasumarthi, Kishore B S

PY - 2003/7

Y1 - 2003/7

N2 - Lower vertebrates such as newt and zebrafish are able to reactivate high levels of cardiomyocyte cell cycle activity in response to experimental injury resulting in apparent regeneration. In contrast, damaged myocardium is replaced by fibrotic scar tissue in higher vertebrates. This process compromises the contractile function of the surviving myocardium, ultimately leading to heart failure. Various strategies are being pursued to augment myocyte number in the diseased hearts. One approach entails the reactivation of cell cycle in surviving cardiomyocytes. Here, we provide a summary of methods to monitor cell cycle activity, and interventions demonstrating positive cell cycle effects in cardiomyocytes as well as discuss the potential utility of cell cycle regulation to augment myocyte number in diseased hearts.

AB - Lower vertebrates such as newt and zebrafish are able to reactivate high levels of cardiomyocyte cell cycle activity in response to experimental injury resulting in apparent regeneration. In contrast, damaged myocardium is replaced by fibrotic scar tissue in higher vertebrates. This process compromises the contractile function of the surviving myocardium, ultimately leading to heart failure. Various strategies are being pursued to augment myocyte number in the diseased hearts. One approach entails the reactivation of cell cycle in surviving cardiomyocytes. Here, we provide a summary of methods to monitor cell cycle activity, and interventions demonstrating positive cell cycle effects in cardiomyocytes as well as discuss the potential utility of cell cycle regulation to augment myocyte number in diseased hearts.

KW - Cardiomyocyte

KW - Cell cycle

KW - Myocardial repair

UR - http://www.scopus.com/inward/record.url?scp=0042564561&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0042564561&partnerID=8YFLogxK

U2 - 10.1023/A:1024738104722

DO - 10.1023/A:1024738104722

M3 - Article

VL - 8

SP - 293

EP - 303

JO - Heart Failure Reviews

JF - Heart Failure Reviews

SN - 1382-4147

IS - 3

ER -