Physiological myocardial hypertrophy: how and why?

被引:75
作者
Catalucci, Daniele [1 ,2 ]
Latronico, Michael V. G. [2 ]
Ellingsen, Oyvind [3 ,4 ]
Condorelli, Gianluigi [1 ,2 ]
机构
[1] Univ Calif San Diego, Dept Med, Div Cardiol, La Jolla, CA 92093 USA
[2] MultiMed Hosp, IRCCS, I-20100 Milan, Italy
[3] Norwegian Univ Sci & Technol, Dept Circulat & Med Imaging, N-7034 Trondheim, Norway
[4] St Olavs Hosp, Dept Cardiol, Trondheim, Norway
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2008年 / 13卷
关键词
heart; hypertrophy; IGF1; Akt; review;
D O I
10.2741/2681
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Cardiac hypertrophy is defined by augmentation of ventricular mass as a result of increased cardiomyocyte size, and is the adaptive response of the heart to enhanced hemodynamic loads due to either physiological stimuli (post-natal developmental growth, training, and pregnancy) or pathological states (such as hypertension, valvular insufficiency, etc). The mechanisms leading to hypertrophy during pathological and physiological states are distinct but, in general, evidence indicates that hypertrophy results from the interaction of mechanical forces and neurohormonal factors. Hemodynamic overload creates a mechanical burden on the heart and results in stretch of the myocyte and induction of gene expression of cardiac growth factors. Insulin-like growth factor 1 (IGF1) has recently been shown to be the most important cardiac growth factor involved in physiological hypertrophy. In this review, IGF1 and the pathways it triggers will be discussed.
引用
收藏
页码:312 / 324
页数:13
相关论文
共 108 条
  • [22] CONDORELLI G, 2002, P NATL ACAD SCI US
  • [23] Regulation of myocardial contractility and cell size by distinct PI3K-PTEN signaling pathways
    Crackower, MA
    Oudit, GY
    Kozieradzki, I
    Sarao, R
    Sun, H
    Sasaki, T
    Hirsch, E
    Suzuki, A
    Shioi, T
    Irie-Sasaki, J
    Sah, R
    Cheng, HYM
    Rybin, VO
    Lembo, G
    Fratta, L
    Oliveira-dos-Santos, AJ
    Benovic, JL
    Kahn, CR
    Izumo, S
    Steinberg, SF
    Wymann, MP
    Backx, PH
    Penninger, JM
    [J]. CELL, 2002, 110 (06) : 737 - 749
  • [24] Akt1 is required for physiological cardiac growth
    DeBosch, B
    Treskov, I
    Lupu, TS
    Weinheimer, C
    Kovacs, A
    Courtois, M
    Muslin, AJ
    [J]. CIRCULATION, 2006, 113 (17) : 2097 - 2104
  • [25] Activation of the cardiac proteasome during pressure overload promotes ventricular hypertrophy
    Depre, Christophe
    Wang, Qian
    Yan, Lin
    Hedhli, Nadia
    Peter, Pallavi
    Chen, Li
    Hong, Chull
    Hittinger, Luc
    Ghaleh, Bijan
    Sadoshima, Junichi
    Vatner, Dorothy E.
    Vatner, Stephen F.
    Madura, Kiran
    [J]. CIRCULATION, 2006, 114 (17) : 1821 - 1828
  • [26] GSK-3: tricks of the trade for a multi-tasking kinase
    Doble, BW
    Woodgett, JR
    [J]. JOURNAL OF CELL SCIENCE, 2003, 116 (07) : 1175 - 1186
  • [27] Cardiovascular and metabolic effects of insulin-like growth factor I at rest and during exercise in humans
    Donath, MY
    Jenni, R
    Brunner, HP
    Anrig, M
    Kohli, S
    Glatz, Y
    Froesch, ER
    [J]. JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1996, 81 (11) : 4089 - 4094
  • [28] PDK2: the missing piece in the receptor tyrosine kinase signaling pathway puzzle
    Dong, LQ
    Liu, F
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2005, 289 (02): : E187 - E196
  • [29] Conditional switching of VEGF provides new insights into adult neovascularization and pro-angiogenic therapy
    Dor, Y
    Djonov, V
    Abramovitch, R
    Itin, A
    Fishman, GI
    Carmeliet, P
    Goelman, G
    Keshet, E
    [J]. EMBO JOURNAL, 2002, 21 (08) : 1939 - 1947
  • [30] Low- and high-level transgenic expression of β2-adrenergic receptors differentially affect cardiac hypertrophy and function in Gαq-overexpressing mice
    Dorn, GW
    Tepe, NM
    Lorenz, JN
    Koch, WJ
    Liggett, SB
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (11) : 6400 - 6405