Modulation of the cardiomyocyte cell cycle in genetically altered animals

被引:27
作者
Field, LJ
机构
[1] Indiana Univ, Sch Med, Krannert Inst Cardiol, Indianapolis, IN 46202 USA
[2] Indiana Univ, Sch Med, Herman B Wells Ctr, Indianapolis, IN 46202 USA
来源
CARDIAC ENGINEERING: FROM GENES AND CELLS TO STRUCTURE AND FUNCTION | 2004年 / 1015卷
关键词
regeneration; proliferation; apoptosis; heart disease;
D O I
10.1196/annals.1302.013
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Many forms of cardiovascular disease are associated with cardiomyocyte loss via apoptosis and/or necrosis. Although there is currently debate regarding the level at which adult cardiomyocytes can reenter the cell cycle and proliferate, it is clear that the intrinsic regenerative growth capacity is insufficient to reverse the progression to failure in badly injured hearts. The ability to reactivate cardiomyocyte proliferation in damaged hearts might permit regenerative growth, provided that the nascent cells are able to participate in a functional syncytium with the surviving myocardium. In this review, techniques commonly used to monitor cardiomyocyte cell cycle activity in normal and injured hearts are discussed. In addition, several genetic models are described wherein the expression of fundamental cell cycle regulatory proteins has been altered in cardiomyocytes.
引用
收藏
页码:160 / 170
页数:11
相关论文
共 43 条
  • [1] [Anonymous], GROWTH HYPERPLASIA C
  • [2] Myocyte renewal and ventricular remodelling
    Anversa, P
    Nadal-Ginard, B
    [J]. NATURE, 2002, 415 (6868) : 240 - 243
  • [3] Ventricular myocytes are not terminally differentiated in the adult mammalian heart
    Anversa, P
    Kajstura, J
    [J]. CIRCULATION RESEARCH, 1998, 83 (01) : 1 - 14
  • [4] HEART AND BONE-TUMORS IN TRANSGENIC MICE
    BEHRINGER, RR
    PESCHON, JJ
    MESSING, A
    GARTSIDE, CL
    HAUSCHKA, SD
    PALMITER, RD
    BRINSTER, RL
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1988, 85 (08) : 2648 - 2652
  • [5] BOUSQUET PF, 1990, CANCER RES, V50, P1431
  • [6] A constitutive mutation of ALK5 disrupts cardiac looping and morphogenesis in mice
    Charng, MJ
    Frenkel, PA
    Lin, Q
    Yumada, M
    Schwartz, RJ
    Olson, EN
    Overbeek, P
    Schneider, MD
    [J]. DEVELOPMENTAL BIOLOGY, 1998, 199 (01) : 72 - 79
  • [7] REQUIREMENT FOR A FUNCTIONAL RB-1 GENE IN MURINE DEVELOPMENT
    CLARKE, AR
    MAANDAG, ER
    VANROON, M
    VANDERLUGT, NMT
    VANDERVALK, M
    HOOPER, ML
    BERNS, A
    RIELE, HT
    [J]. NATURE, 1992, 359 (6393) : 328 - 330
  • [8] CLUBB FJ, 1984, LAB INVEST, V50, P571
  • [9] IDENTIFICATION OF SV40 LARGE T-ANTIGEN-ASSOCIATED PROTEINS IN CARDIOMYOCYTES FROM TRANSGENIC MICE
    DAUD, AI
    LANSON, NA
    CLAYCOMB, WC
    FIELD, LJ
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY, 1993, 264 (05): : H1693 - H1700
  • [10] A method to score micronuclei in vivo using cytochalasin B-induced cytokinesis block
    Devi, PU
    Rao, BSS
    Kamath, R
    [J]. MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS, 1998, 401 (1-2) : 33 - 37