粒体自噬
线粒体
氧化应激
端粒
生物
线粒体DNA
衰老
串扰
线粒体生物发生
老化
细胞生物学
生物信息学
自噬
内分泌学
遗传学
细胞凋亡
基因
物理
光学
作者
Yu-juan Li,Xiao Jin,Dan Li,Jing Lu,Xiao-nan Zhang,Sheng-jie Yang,Yi-xi Zhao,Min Wu
标识
DOI:10.1016/j.biopha.2022.113954
摘要
Vascular aging, a major risk factor for cardiovascular disease, contributes to morbidity and mortality in older people. Mitochondria play an important role in vascular aging. In endothelial and smooth muscle cells, multiple changes in the mitochondrial structure and function contribute to aging, including the effects of mitochondrial oxidative stress, mitochondrial DNA mutations, mitochondrial dynamics, and mitophagy. Mitochondrial dysfunction also contributes to other age-related molecular and cellular mechanisms, such as crosstalk with telomeres, senescence-associated secretory phenotypes, and low-grade inflammation. Thus, enhancing mitochondrial biogenesis, reducing oxidative stress, recovering dynamics, and mitophagy have been suggested as effective interventions to delay vascular aging and age-related cardiovascular diseases. Furthermore, accumulating evidence has shown that commonly used herbs and their natural compounds have great potential to improve mitochondrial function during vascular aging. Herein, we review the cellular and molecular mechanisms of mitochondrial effects on vascular aging, emphasizing the efficacy of natural compounds in the treatment of vascular aging by improving mitochondrial structure and function. We aim to provide new insights into delaying vascular aging and preventing cardiovascular diseases. • Mitochondrial dysfunction contributes to vascular aging, adversely affecting the health and longevity of the elderly. • Oxidative stress and dysfunction of mitochondrial DNA, dynamics and mitophagy can be found in senescent ECs and VSMCs. • Similar structure and crosstalk between mitochondria and telomeres together facilitate vascular aging. • Natural compounds from herbal medicine have great potential to improve mitochondrial function and delay vascular aging.
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