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Endocrine, Metabolic & Immune Disorders - Drug Targets

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ISSN (Online): 2212-3873

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Review Article

The Emerging Roles of IL-36, IL-37, and IL-38 in Diabetes Mellitus and its Complications

Author(s): Guoqing Huang, Mingcai Li, Xiaoqing Tian, Qiankai Jin, Yushan Mao* and Yan Li*

Volume 22, Issue 10, 2022

Published on: 15 June, 2022

Page: [997 - 1008] Pages: 12

DOI: 10.2174/1871530322666220113142533

Price: $65

Abstract

Diabetes mellitus is a metabolic disease caused by a combination of genetic and environmental factors. The importance of the inflammatory response occurring in the pancreas and adipose tissue in the occurrence and progression of diabetes has been gradually accepted. Excess blood glucose and free fatty acids produce large amounts of inflammatory cytokines and chemokines through oxidative stress and endoplasmic reticulum stress. There is sufficient evidence that proinflammatory mediators, such as interleukin (IL)-1β, IL-6, macrophage chemotactic protein-1, and tumor necrosis factor-α, are engaged in insulin resistance in peripheral adipose tissue and the apoptosis of pancreatic β-cells. IL-36, IL-37, and IL-38, as new members of the IL-1 family, play an indispensable role in the regulation of immune system homeostasis and are involved in the pathogenesis of inflammatory and autoimmune diseases. Recently, the abnormal expression of IL-36, IL-37, and IL-38 in diabetes has been reported. In this review, we discuss the emerging functions, potential mechanisms, and future research directions on the role of IL-36, IL-37, and IL-38 in diabetes mellitus and its complications.

Keywords: Diabetes mellitus, complications, inflammation, IL-36, IL-37, IL-38.

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