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慢性压力与加速衰老之间的联系。

The Link between Chronic Stress and Accelerated Aging.

作者信息

Yegorov Yegor E, Poznyak Anastasia V, Nikiforov Nikita G, Sobenin Igor A, Orekhov Alexander N

机构信息

Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow 119991, Russia.

Institute for Atherosclerosis Research, Skolkovo Innovative Center, Moscow 121609, Russia.

出版信息

Biomedicines. 2020 Jul 7;8(7):198. doi: 10.3390/biomedicines8070198.

DOI:10.3390/biomedicines8070198
PMID:32645916
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7400286/
Abstract

People exposed to chronic stress age rapidly. The telomeres in their cells of all types shorten faster. Inflammation is another important feature of stress that, along with aging, accounts for the phenomenon of inflammaging. In addition to aging itself, inflammaging can contribute to the development of several pathologies, including atherosclerosis, diabetes, hypertension, and others. Oxidative stress is one of the main mechanisms related to stress. Oxidative stress is caused by the over-production of reactive oxygen species (ROS) that can damage various tissues. The main source of ROS is mitochondria. Being suppressed by mitochondrial mutations, mitophagy can aggravate the situation. In this case, the aging-specific pro-inflammatory changes are amplified. It happens because of the inability of cells to maintain the normal state of mitochondria. Macrophages are the crucial element of the innate immunity associated with the chronic inflammation and, subsequently, with the inflammaging. In this review, we focus on the therapy approaches potentially reducing the deleterious effects of oxidative stress. These include stimulation of mitophagy, activation of mitochondrial uncoupling, induction of the expression of the telomerase catalytic component gene, and use of antioxidants. Any method reducing oxidative stress should improve post-traumatic stress disorder.

摘要

长期处于压力下的人衰老速度加快。他们各类细胞中的端粒缩短得更快。炎症是压力的另一个重要特征,与衰老一起导致了炎症衰老现象。除了衰老本身,炎症衰老还会促使包括动脉粥样硬化、糖尿病、高血压等多种疾病的发展。氧化应激是与压力相关的主要机制之一。氧化应激是由活性氧(ROS)产生过多引起的,活性氧会损害各种组织。活性氧的主要来源是线粒体。线粒体自噬受到线粒体突变的抑制,会使情况恶化。在这种情况下,衰老特异性的促炎变化会加剧。这是因为细胞无法维持线粒体的正常状态。巨噬细胞是先天免疫的关键要素,与慢性炎症以及随后的炎症衰老相关。在这篇综述中,我们重点关注可能减轻氧化应激有害影响的治疗方法。这些方法包括刺激线粒体自噬、激活线粒体解偶联、诱导端粒酶催化成分基因的表达以及使用抗氧化剂。任何减轻氧化应激的方法都应能改善创伤后应激障碍。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37e4/7400286/03d5b04699a3/biomedicines-08-00198-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37e4/7400286/1785327738bc/biomedicines-08-00198-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37e4/7400286/03d5b04699a3/biomedicines-08-00198-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37e4/7400286/1785327738bc/biomedicines-08-00198-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37e4/7400286/03d5b04699a3/biomedicines-08-00198-g002.jpg

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Mitochondria, Telomeres and Telomerase Subunits.线粒体、端粒与端粒酶亚基
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