Cardiac aging in mice and humans: the role of mitochondrial oxidative stress.
Cardiac aging in mice and humans: the role of mitochondrial oxidative stress.
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DOI:
10.1016/j.tcm.2009.12.004
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发表时间:
2009-10
影响因子:
9.3
通讯作者:
Rabinovitch, Peter S.
中科院分区:
文献类型:
--
作者:
Dai, Dao-Fu;Rabinovitch, Peter S.
Age is a major risk factor for cardiovascular diseases, not only because it prolongs exposure to several other cardiovascular risks, but also owing to intrinsic cardiac aging, which reduces cardiac functional reserve, predisposes the heart to stress and contributes to increased cardiovascular mortality in the elderly. Intrinsic cardiac aging in the murine model closely recapitulates age-related cardiac changes in humans, including left ventricular hypertrophy, fibrosis and diastolic dysfunction. Cardiac aging in mice is accompanied by accumulation of mitochondrial protein oxidation, increased mitochondrial DNA mutations, increased mitochondrial biogenesis, as well as decreased cardiac SERCA2 protein. All of these age-related changes are significantly attenuated in mice overexpressing catalase targeted to mitochondria (mCAT). These findings demonstrate the critical role of mitochondrial reactive oxygen species (ROS) in cardiac aging and support the potential application of mitochondrial antioxidants to cardiac aging and age-related cardiovascular diseases.
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影响因子:
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通讯作者:
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