Islet β cell dedifferentiation in pathogenesis of type 2 diabetes
10.3969/j.issn.1000-4718.2024.03.018
- VernacularTitle:胰岛β细胞去分化与2型糖尿病
- Author:
Maosen ZHANG
1
;
Hai ZHANG
;
Weiping ZHANG
Author Information
1. 海军军医大学病理生理学教研室,上海 200433
- Keywords:
type 2 diabetes;
islet β cells;
dedifferentiation;
insulin
- From:
Chinese Journal of Pathophysiology
2024;40(3):535-542
- CountryChina
- Language:Chinese
-
Abstract:
Insulin secretion by islet β cells is a fundamental component in glucose homeostasis.Chronic meta-bolic stress causes β cell dysfunction as manifested by reduced cell mass and impaired insulin secretion,which contributes to the pathogenesis of type 2 diabetes(T2D).In the last decade,it has been putatively accepted that β cell dedifferentia-tion is a key pathological mechanism for β cell failure.β cell dedifferentiation is referred as the progressive process that β cells lose their identity and dedifferentiate into non-functional endocrine progenitor-like cells.Typically,aldehyde dehy-drogenase 1 family member A3(ALDH1A3)is a marker of β cell dedifferentiation.Chronic hyperglycemia can lead to de-differentiation of mature β cells,the mechanism of which involves oxidative stress and some key factors.β cell dedifferen-tiation is reversible,therefore,to intervene this process may represent a promising approach to the restoration of β cell function.In this review,we update the recent progress in the pathophysiology of β cell dedifferentiation to provide new strategy for the prevention and treatment of T2D.
