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Review
. 2012 Apr 13;110(8):1109-24.
doi: 10.1161/CIRCRESAHA.111.246140.

Mitochondria and cardiovascular aging

Dao-Fu Dai  1 , Peter S Rabinovitch, Zoltan Ungvari
Affiliations
Review

Mitochondria and cardiovascular aging

Dao-Fu Dai et al. Circ Res. .

Abstract

Old age is a major risk factor for cardiovascular diseases. Several lines of evidence in experimental animal models have indicated the central role of mitochondria both in lifespan determination and in cardiovascular aging. In this article we review the evidence supporting the role of mitochondrial oxidative stress, mitochondrial damage and biogenesis as well as the crosstalk between mitochondria and cellular signaling in cardiac and vascular aging. Intrinsic cardiac aging in the murine model closely recapitulates age-related cardiac changes in humans (left ventricular hypertrophy, fibrosis and diastolic dysfunction), while the phenotype of vascular aging include endothelial dysfunction, reduced vascular elasticity, and chronic vascular inflammation. Both cardiac and vascular aging involve neurohormonal signaling (eg, renin-angiotensin, adrenergic, insulin-IGF1 signaling) and cell-autonomous mechanisms. The potential therapeutic strategies to improve mitochondrial function in aging and cardiovascular diseases are also discussed, with a focus on mitochondrial-targeted antioxidants, calorie restriction, calorie restriction mimetics, and exercise training.

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Figures

Figure 1
Figure 1
Proposed signaling mechanism of Angiotensin/Gαq and mitochondrial ROS amplification in aging and cardiovascular diseases. AT1-R = angiotensin receptor-1; Nnt = nicotinamide nucleotide transferase
Figure 2
Figure 2
Summary of mitochondrial-targeted interventions and their therapeutic potential in aging. xCT= cysteine transporter
See this image and copyright information in PMC

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