title: Endoplasmic reticulum stress is involved in the connection between inflammation and autophagy in type 2 diabetes.
abstract: Type 2 diabetes is a chronic inflammatory disease. A number of studies have clearly demonstrated that cytokines such as interleukin 1β (IL1β) contribute to pancreatic inflammation, leading to impaired glucose homeostasis and diabetic disease. There are findings which suggest that islet β-cells can secrete cytokines and cause inflammatory responses. In this process, thioredoxin-interacting protein (TXNIP) is induced by endoplasmic reticulum (ER) stress, which further demonstrates a potential role for ER stress in innate immunity via activation of the NOD-like receptor (NLRP) 3/caspase1 inflammasome and in diabetes pathogenesis via the release of cytokines. Recent developments have also revealed a crucial role for the autophagy pathway during ER stress and inflammation. Autophagy is an intracellular catabolic system that not only plays a crucial role in maintaining the normal islet architecture and intracellular insulin content but also represents a form of programmed cell death. In this review, we focus on the roles of autophagy, inflammation, and ER stress in type 2 diabetes but, above all, on the connections among these factors.
authors.affiliation: Department of Endocrinology, The First Affiliated Hospital of Harbin Medical University, No. 23 You zheng Street Nan Gang District, Harbin 150001, China.
authors.forename: Han
authors.initials: H
authors.lastname: Liu
authors.affiliation: Department of Endocrinology, The First Affiliated Hospital of Harbin Medical University, No. 23 You zheng Street Nan Gang District, Harbin 150001, China.
authors.forename: Ming-ming
authors.initials: MM
authors.lastname: Cao
authors.affiliation: Department of Endocrinology, The First Affiliated Hospital of Harbin Medical University, No. 23 You zheng Street Nan Gang District, Harbin 150001, China.
authors.forename: Yang
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Endocrinology, The First Affiliated Hospital of Harbin Medical University, No. 23 You zheng Street Nan Gang District, Harbin 150001, China.
authors.forename: Le-chen
authors.initials: LC
authors.lastname: Li
authors.affiliation: Department of Endocrinology, The First Affiliated Hospital of Harbin Medical University, No. 23 You zheng Street Nan Gang District, Harbin 150001, China.
authors.forename: Li-bo
authors.initials: LB
authors.lastname: Zhu
authors.affiliation: Department of Endocrinology, The First Affiliated Hospital of Harbin Medical University, No. 23 You zheng Street Nan Gang District, Harbin 150001, China.
authors.forename: Guang-ying
authors.initials: GY
authors.lastname: Xie
authors.affiliation: Department of Endocrinology, The First Affiliated Hospital of Harbin Medical University, No. 23 You zheng Street Nan Gang District, Harbin 150001, China. Electronic address: liyanbo5637@163.com.
authors.forename: Yan-bo
authors.initials: YB
authors.lastname: Li
mesh_terms: D000818:Animals; D001343:Autophagy / Q000502:physiology*; D003924:Diabetes Mellitus, Type 2 / Q000209:etiology / Q000503:physiopathology*; D059865:Endoplasmic Reticulum Stress / Q000502:physiology*; D006801:Humans; D007249:Inflammation / Q000150:complications / Q000378:metabolism / Q000503:physiopathology; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance / Q000502:physiology
chemical_list: D007328:Insulin
keywords: Autophagy; Endoplasmic reticulum stress; Inflammation; Interleukin 1β; Type 2 diabetes