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衰老过程中慢性炎症的来源。

Source of Chronic Inflammation in Aging.

作者信息

Sanada Fumihiro, Taniyama Yoshiaki, Muratsu Jun, Otsu Rei, Shimizu Hideo, Rakugi Hiromi, Morishita Ryuichi

机构信息

Department of Clinical Gene Therapy, Graduate School of Medicine, Osaka University, Suita, Japan.

Department of Geriatric and General Medicine, Graduate School of Medicine, Osaka University, Suita, Japan.

出版信息

Front Cardiovasc Med. 2018 Feb 22;5:12. doi: 10.3389/fcvm.2018.00012. eCollection 2018.

Abstract

Aging is a complex process that results from a combination of environmental, genetic, and epigenetic factors. A chronic pro-inflammatory status is a pervasive feature of aging. This chronic low-grade inflammation occurring in the absence of overt infection has been defined as "inflammaging" and represents a significant risk factor for morbidity and mortality in the elderly. The low-grade inflammation persists even after reversing pro-inflammatory stimuli such as LDL cholesterol and the renin-angiotensin system (RAS). Recently, several possible sources of chronic low-grade inflammation observed during aging and age-related diseases have been proposed. Cell senescence and dysregulation of innate immunity is one such mechanism by which persistent prolonged inflammation occurs even after the initial stimulus has been removed. Additionally, the coagulation factor that activates inflammatory signaling beyond its role in the coagulation system has been identified. This signal could be a new source of chronic inflammation and cell senescence. Here, we summarized the factors and cellular pathways/processes that are known to regulate low-grade persistent inflammation in aging and age-related disease.

摘要

衰老 是一个复杂的过程,由环境、遗传和表观遗传因素共同作用导致。慢性促炎状态是衰老的一个普遍特征。这种在无明显感染情况下发生的慢性低度炎症被定义为“炎症衰老”,是老年人发病和死亡的一个重要危险因素。即使在逆转诸如低密度脂蛋白胆固醇和肾素 - 血管紧张素系统(RAS)等促炎刺激后,低度炎症仍会持续。最近,有人提出了衰老和与年龄相关疾病期间观察到的慢性低度炎症的几种可能来源。细胞衰老和先天免疫失调就是这样一种机制,即使在初始刺激消除后,仍会发生持续的长期炎症。此外,已确定了在凝血系统作用之外激活炎症信号的凝血因子。该信号可能是慢性炎症和细胞衰老的一个新来源。在此,我们总结了已知在衰老和与年龄相关疾病中调节低度持续性炎症的因素及细胞途径/过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fe3/5850851/a6fe4c272bbe/fcvm-05-00012-g001.jpg

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