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衰老科学交叉点上的元炎症衰老

Meta-inflammaging at the crossroad of geroscience.

作者信息

Chen Guobing, Yung Raymond

机构信息

Institute of Geriatric Immunology School of Medicine Jinan University Guangzhou China.

Department of Microbiology and Immunology School of Medicine Jinan University Guangzhou China.

出版信息

Aging Med (Milton). 2019 Sep 8;2(3):157-161. doi: 10.1002/agm2.12078. eCollection 2019 Sep.

DOI:10.1002/agm2.12078
PMID:31942529
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6880720/
Abstract

Geroscience posits that selected fundamental biological processes are the foundation of age-related chronic diseases and are responsible for the decline in physical and mental function in old age. Late-life chronic low-grade inflammation ("inflammaging") and altered signal transduction pathways in metabolism have been identified as two of the key themes in the aging process. Age-related changes in the immune and metabolic responses are also recognized as playing a critical pathogenic role in most common chronic medical conditions that plague the elderly. Emerging investigations emphasize the interconnectedness of the immune and metabolic responses in aging, an area of gerontological research that can be termed "meta-inflammaging."

摘要

老年科学认为,特定的基本生物学过程是与年龄相关的慢性疾病的基础,也是老年身心功能衰退的原因。晚年慢性低度炎症(“炎症衰老”)和代谢中信号转导途径的改变已被确定为衰老过程中的两个关键主题。免疫和代谢反应的年龄相关变化也被认为在困扰老年人的大多数常见慢性疾病中起着关键的致病作用。新出现的研究强调了衰老过程中免疫和代谢反应的相互联系,这一老年学研究领域可称为“元炎症衰老”。

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本文引用的文献

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Complement component C5a induces aberrant epigenetic modifications in renal tubular epithelial cells accelerating senescence by Wnt4/βcatenin signaling after ischemia/reperfusion injury.补体成分C5a在缺血/再灌注损伤后通过Wnt4/β-连环蛋白信号通路诱导肾小管上皮细胞发生异常表观遗传修饰,加速细胞衰老。
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