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[血管衰老的分子机制:细胞衰老对血管平滑肌细胞钙化的影响]

[Molecular mechanism of vascular aging: impact of vascular smooth muscle cell calcification via cellular senescence].

作者信息

Takemura Aya, Iijima Katsuya, Ouchi Yasuyoshi

机构信息

Department of Geriatric Medicine, University of Tokyo.

出版信息

Clin Calcium. 2010 Nov;20(11):1646-55.

PMID:21037384
Abstract

Atherosclerotic vascular damage associated with aging manifest several features, namely atherosis, sclerosis and calcified change, finally leading to cardiovascular (CV) events. Accumulating recent reports show the importance of cellular senescence in atherosclerogenesis; however, few reports have addressed whether cellular senescence is associated with smooth muscle cells (SMC) calcification. Recent report has demonstrated the association of senescent phenotypic change with osteoblastic trans-differentiation in VSMC. In addition, our new findings show that the possibility of dynamic action of sirtuin, which is well known as a longevity gene, as a negative regulator in the cellular senescence-related vascular calcification. Strategies how to manage senescent phenotypic change in VSMC may provide novel therapeutic opportunities for the prevention of vascular calcification.

摘要

与衰老相关的动脉粥样硬化性血管损伤表现出多种特征,即动脉粥样化、硬化和钙化改变,最终导致心血管(CV)事件。最近越来越多的报告表明细胞衰老在动脉粥样硬化发生过程中的重要性;然而,很少有报告探讨细胞衰老是否与平滑肌细胞(SMC)钙化有关。最近的报告已经证明衰老表型变化与血管平滑肌细胞(VSMC)中的成骨细胞转分化有关。此外,我们的新发现表明,作为一种著名的长寿基因,沉默调节蛋白作为细胞衰老相关血管钙化的负调节因子具有动态作用的可能性。如何控制VSMC衰老表型变化的策略可能为预防血管钙化提供新的治疗机会。

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Functional changes of the coronary microvasculature with aging regarding glucose tolerance, energy metabolism, and oxidative stress.随着年龄增长,冠状动脉微血管在葡萄糖耐量、能量代谢和氧化应激方面的功能变化。
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