Review Volume 11, Issue 21 pp 9947—9959
Aging and stress induced β cell senescence and its implication in diabetes development
- 1 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
- 2 Department of Dermatology, The People’s Hospital of Shishou City, Shishou, Hubei, China
- 3 Shenzhen Third People’s Hospital, Longgang District, Shenzhen, Guangdong, China
- 4 Diabetes Center, The Second Xiangya Hospital, Institute of Metabolism and Endocrinology, Central South University, Changsha, China
received: August 15, 2019 ; accepted: October 28, 2019 ; published: November 13, 2019 ;https://doi.org/10.18632/aging.102432
How to Cite
Copyright © 2019 Li et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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.
SASP: senescence associated secretory phenotype; Rb: retinoblastoma protein; SAHF: senescence associated heterochromatin foci; LB: Lipofuscin body; PTTG: Pituitary tumor transforming gene; PDGF: Platelet-derived growth factor; GLP-1R: glucagon like peptide 1 receptor; NFAT: nuclear factor of activated T cells; BMI1: B lymphoma M0-MLV insertion region1 homolog; EZH2: enhancer of zeste homolog2; TDP: Time-dependent potentiation; SMP-30: senescence marker protein-30; GSIS: glucose stimulated insulin secretion; FLIM: fluorescence lifetime imaging; NOD: non-obese diabetic mice.