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衰老和应激诱导的β细胞衰老及其在糖尿病发生中的意义。

Aging and stress induced β cell senescence and its implication in diabetes development.

作者信息

Li Na, Liu Furong, Yang Ping, Xiong Fei, Yu Qilin, Li Jinxiu, Zhou Zhiguang, Zhang Shu, Wang Cong-Yi

机构信息

The Center for Biomedical Research, Key Laboratory of Organ Transplantation, Ministry of Education, NHC Key Laboratory of Organ Transplantation, Key Laboratory of Organ Transplantation, Chinese Academy of Medical Sciences, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Department of Dermatology, The People's Hospital of Shishou City, Shishou, Hubei, China.

出版信息

Aging (Albany NY). 2019 Nov 13;11(21):9947-9959. doi: 10.18632/aging.102432.

DOI:10.18632/aging.102432
PMID:31721726
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6874445/
Abstract

Cellular senescence is a well-established defensive mechanism for tumor suppression, and is also proposed to play a crucial role in embryonic development, wound repair, aging and age-related diseases. Senescent cell is characterized by the marked morphological changes and active metabolism along with a distinctive senescence associated secretion phenotype (SASP). Cellular senescence is triggered by multiple endogenous and exogenous stressors, which collectively induce three types of senescence. It is believed that senescence represents a programmed phenomenon to facilitate β cell functional maturation and, therefore, senescence has been suggested to be involved in β cell regeneration, insulin secretion and diabetes development. Nevertheless, despite past extensive studies, the exact impact of senescence on β cell viability, regeneration and functionality, and its relevance to the development of diabetes are yet to be fully addressed. In this review, we will summarize the recent progress in β cell senescence, through which we intend to spark more instructive discussion and perspective with regard to the mechanisms underlying β cell senescence and their links to the pathogenesis of diabetes and the development of therapeutic strategies.

摘要

细胞衰老作为一种成熟的肿瘤抑制防御机制,也被认为在胚胎发育、伤口修复、衰老及衰老相关疾病中发挥关键作用。衰老细胞具有显著的形态变化、活跃的代谢以及独特的衰老相关分泌表型(SASP)。细胞衰老由多种内源性和外源性应激源触发,这些应激源共同诱导三种类型的衰老。人们认为衰老代表一种程序性现象,有助于β细胞功能成熟,因此,衰老被认为与β细胞再生、胰岛素分泌及糖尿病发展有关。然而,尽管过去进行了广泛研究,但衰老对β细胞活力、再生和功能的确切影响及其与糖尿病发展的相关性仍有待充分阐明。在本综述中,我们将总结β细胞衰老的最新进展,借此引发更多关于β细胞衰老机制及其与糖尿病发病机制和治疗策略发展之间联系的有启发性的讨论和观点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a213/6874445/a6ac4e073a96/aging-11-102432-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a213/6874445/35f0956c89ec/aging-11-102432-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a213/6874445/a6ac4e073a96/aging-11-102432-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a213/6874445/35f0956c89ec/aging-11-102432-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a213/6874445/a6ac4e073a96/aging-11-102432-g002.jpg

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