Mitochondria and cardiovascular aging.
Mitochondria and cardiovascular aging.
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DOI：
10.1161/circresaha.111.246140
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发表时间：
2012-04-13
影响因子：
20.1
通讯作者：
Ungvari Z
中科院分区：
文献类型：
--
作者：
Dai DF;Rabinovitch PS;Ungvari Z
老年是心血管疾病的主要危险因素。实验动物模型中的几条证据表明线粒体在寿命决定和心血管衰老中的核心作用。在这篇文章中，我们回顾了支持线粒体氧化应激，线粒体损伤和生物发生的作用，以及线粒体和细胞信号之间的串扰在心脏和血管老化的证据。鼠模型中的内在心脏衰老密切地再现了人类中与年龄相关的心脏变化（左心室肥大、纤维化和舒张功能障碍），而血管衰老的表型包括内皮功能障碍、血管弹性降低和慢性血管炎症。心脏和血管老化均涉及神经激素信号传导（例如，肾素-血管紧张素、肾上腺素能、胰岛素-IGF 1信号传导）和细胞自主机制。还讨论了改善衰老和心血管疾病中线粒体功能的潜在治疗策略，重点是针对肾脏的抗氧化剂，热量限制，热量限制模拟物和运动训练。
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 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 (e.g. 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.