Views from within and beyond - Narratives of cardiac contractile dysfunction under senescence

被引:42
作者
Yang, XP
Sreejayan, N
Ren, J [1 ]
机构
[1] Univ Wyoming, Div Pharmaceut Sci, Laramie, WY 82071 USA
[2] Univ Wyoming, Ctr Cardiovasc Res & Alternat Med, Laramie, WY 82071 USA
关键词
age; stress signaling; cardiac; contractile function;
D O I
10.1385/ENDO:26:2:127
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Senesecence is associated with enhanced risk of cardiovascular diseases. It is generally considered that decline in growth hormones (such as insulin-like growth factor I), intrinsic myocardial and endothelial functions, as well as accumuation of reactive oxygen species with increased age may contribute to cardiovascular senescence. It is believed that heart function, especially cardiac reserve declines with advanced age. However, most experimental and clinical investigations on ventricluar function only included young or adult subjects and failed to address this important age issue in heart pathophysiology. Although senescent but otherwise healthy hearts may possess normal pumping function at the resting or non-stressed state, some aging-associated factors such as accumulation of reactive oxygen species and activation of selective stress signaling pathways may interact with certain risk factors and compromise overall cardiac function. The precise cause and progression of compromised cardiac function in the elderly remain controversial. This review will focus on senescene-related alterations in cardiac contractile function with a special emphasis on oxidative stress and activation of stress signaling.
引用
收藏
页码:127 / 137
页数:11
相关论文
共 168 条
[1]   Mitochondrial DNA and aging [J].
Alexeyev, MF ;
LeDoux, SP ;
'Wilson, GL .
CLINICAL SCIENCE, 2004, 107 (04) :355-364
[2]   Age-dependent expression of fibrosis-related genes and collagen deposition in the rat myocardium [J].
Annoni, G ;
Luvarà, G ;
Arosio, B ;
Gagliano, N ;
Fiordaliso, F ;
Santambrogio, D ;
Jeremic, G ;
Mircoli, L ;
Latini, R ;
Vergani, C ;
Masson, S .
MECHANISMS OF AGEING AND DEVELOPMENT, 1998, 101 (1-2) :57-72
[3]  
[Anonymous], NOVARTIS FDN S
[4]  
[Anonymous], NOVARTIS FDN S
[5]   Aging-related increase in oxidative stress correlates with developmental pattern of beta-secretase activity and beta-amyloid plaque formation in transgenic Tg2576 mice with Alzheimer-like pathology [J].
Apelt, J ;
Bigl, M ;
Wunderlich, P ;
Schliebs, R .
INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE, 2004, 22 (07) :475-484
[6]   An advanced glycation endproduct cross-link breaker can reverse age-related increases in myocardial stiffness [J].
Asif, M ;
Egan, J ;
Vasan, S ;
Jyothirmayi, GN ;
Masurekar, MR ;
Lopez, S ;
Williams, C ;
Torres, RL ;
Wagle, D ;
Ulrich, P ;
Cerami, A ;
Brines, M ;
Regan, TJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (06) :2809-2813
[7]   When cells get stressed: an integrative view of cellular senescence [J].
Ben-Porath, I ;
Weinberg, RA .
JOURNAL OF CLINICAL INVESTIGATION, 2004, 113 (01) :8-13
[8]   Cardiovascular effects of GH [J].
Bengtsson, BA ;
Christiansen, JS ;
Cuneo, RC ;
Sacca, L .
JOURNAL OF ENDOCRINOLOGY, 1997, 152 (01) :1-3
[9]   Extension of life-span by introduction of telomerase into normal human cells [J].
Bodnar, AG ;
Ouellette, M ;
Frolkis, M ;
Holt, SE ;
Chiu, CP ;
Morin, GB ;
Harley, CB ;
Shay, JW ;
Lichtsteiner, S ;
Wright, WE .
SCIENCE, 1998, 279 (5349) :349-352
[10]   Living and dying for sex - A theory of aging based on the modulation of cell cycle signaling by reproductive hormones [J].
Bowen, RL ;
Atwood, CS .
GERONTOLOGY, 2004, 50 (05) :265-290