Mitochondrial damage-associated molecular patterns: A new insight into metabolic inflammation in type 2 diabetes mellitus.

Abstract

The pathogenesis of diabetes is accompanied by increased levels of inflammatory factors, also known as "metabolic inflammation", which runs through the whole process of the occurrence and development of the disease. Mitochondria, as the key site of glucose and lipid metabolism, is often accompanied by mitochondrial function damage in type 2 diabetes mellitus (T2DM). Damaged mitochondria release pro-inflammatory factors through damage-related molecular patterns that activate inflammation pathways and reactions to oxidative stress, further aggravate metabolic disorders, and form a vicious circle. Currently, the pathogenesis of diabetes is still unclear, and clinical treatment focuses primarily on symptomatic intervention of the internal environment of disorders of glucose and lipid metabolism with limited clinical efficacy. The proinflammatory effect of mitochondrial damage-associated molecular pattern (mtDAMP) in T2DM provides a new research direction for exploring the pathogenesis and intervention targets of T2DM. Therefore, this review covers the most recent findings on the molecular mechanism and related signalling cascades of inflammation caused by mtDAMP in T2DM and discusses its pathogenic role of it in the pathological process of T2DM to search potential intervention targets.

• Authors: Yan Wang, Jingwu Wang, Si-Yu Tao, Zhengting Liang, Rong Xie, Nan-Nan Liu, Ruxue Deng, Yuelin Zhang, Deqiang Deng, Guangjian Jiang
• Journal: Diabetes/metabolism research and reviews (Diabetes Metab Res Rev) Vol. 40 Issue 2 Pg. e3733 (Feb 2024) ISSN: 1520-7560 [Electronic] England
• PMID: 37823338 (Publication Type: Journal Article, Review)
• Copyright: © 2023 The Authors. Diabetes/Metabolism Research and Reviews published by John Wiley & Sons Ltd.

Chemical References

• Glucose

Topics

• Humans
• Diabetes Mellitus, Type 2 (drug therapy)
• Mitochondria (metabolism, pathology)
• Inflammation (metabolism)
• Glucose (metabolism)
• Signal Transduction
• Insulin Resistance