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
[11]   LOSS OF CIRCADIAN RHYTHMICITY IN BLOOD TESTOSTERONE LEVELS WITH AGING IN NORMAL MEN [J].
BREMNER, WJ ;
VITIELLO, MV ;
PRINZ, PN .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1983, 56 (06) :1278-1281
[12]   INK4a-deficient human diploid fibroblasts are resistant to RAS-induced senescence [J].
Brookes, S ;
Rowe, J ;
Ruas, M ;
Llanos, S ;
Clark, PA ;
Lomax, M ;
James, MC ;
Vatcheva, R ;
Bates, S ;
Vousden, KH ;
Parry, D ;
Gruis, N ;
Smit, N ;
Bergman, W ;
Peters, G .
EMBO JOURNAL, 2002, 21 (12) :2936-2945
[13]   Dwarf mice and the ageing process [J].
BrownBorg, HM ;
Borg, KE ;
Meliska, CJ ;
Bartke, A .
NATURE, 1996, 384 (6604) :33-33
[14]   The mitochondrial-lysosomal axis theory of aging - Accumulation of damaged mitochondria as a result of imperfect autophagocytosis [J].
Brunk, UT ;
Terman, A .
EUROPEAN JOURNAL OF BIOCHEMISTRY, 2002, 269 (08) :1996-2002
[15]   Cardiac stem cells fail with aging - A new mechanism for the age-dependent decline in cardiac function [J].
Capogrossi, MC .
CIRCULATION RESEARCH, 2004, 94 (04) :411-413
[16]   A critical analysis of the role of growth hormone and IGF-1 in aging and lifespan [J].
Carter, CS ;
Ramsey, MM ;
Sonntag, WE .
TRENDS IN GENETICS, 2002, 18 (06) :295-301
[17]   Age-dependent expression of advanced glycation end product receptor genes in the human heart [J].
Casselmann, C ;
Reimann, A ;
Friedrich, I ;
Schubert, A ;
Silber, RE ;
Simm, A .
GERONTOLOGY, 2004, 50 (03) :127-134
[18]   Oxidative stress in cardiovascular disease: myth or fact? [J].
Ceconi, C ;
Boraso, A ;
Cargnoni, A ;
Ferrari, R .
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 2003, 420 (02) :217-221
[19]  
Cesari M, 2004, J GERONTOL A-BIOL, V59, P242
[20]   Oxidative stress-mediated cardiac cell death is a major determinant of ventricular dysfunction and failure in dog dilated cardiomyopathy [J].
Cesselli, D ;
Jakoniuk, I ;
Barlucchi, L ;
Beltrami, AP ;
Hintze, TH ;
Nadal-Ginard, B ;
Kajstura, J ;
Leri, A ;
Anversa, P .
CIRCULATION RESEARCH, 2001, 89 (03) :279-286