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Cardiac aging in mice and humans: the role of mitochondrial oxidative stress
Journal article   Open access   Peer reviewed

Cardiac aging in mice and humans: the role of mitochondrial oxidative stress

Dao-Fu Dai and Peter S Rabinovitch
Trends in cardiovascular medicine, Vol.19(7), pp.213-220
10/2009
DOI: 10.1016/j.tcm.2009.12.004
PMCID: PMC2858758
PMID: 20382344
url
https://doi.org/10.1016/j.tcm.2009.12.004View
Published (Version of record) Open Access

Abstract

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. These findings demonstrate the critical role of mitochondrial reactive oxygen species in cardiac aging and support the potential application of mitochondrial antioxidants to cardiac aging and age-related cardiovascular diseases.
Heart - physiopathology Endocrine System - physiology Mitochondria, Heart - metabolism Reactive Oxygen Species - metabolism Heart Diseases - physiopathology Antioxidants - metabolism Oxidative Stress - physiology Oxidative Stress - genetics Animals Heart Diseases - therapy Mice Receptors, Adrenergic - physiology Mitochondria, Heart - genetics Aging - metabolism

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