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肥胖炎症引起的骨骼肌变化作为纤维化的关键途径:机制与干预策略思考

The Change of Skeletal Muscle Caused by Inflammation in Obesity as the Key Path to Fibrosis: Thoughts on Mechanisms and Intervention Strategies.

作者信息

Li Yixuan, Guo Wenwen, Li Han, Wang Yuhao, Liu Xinwei, Kong Wen

机构信息

Department of Endocrinology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.

Diabetes and Metabolic Disease Clinical Research Center of Hubei Province, Wuhan 430022, China.

出版信息

Biomolecules. 2024 Dec 27;15(1):20. doi: 10.3390/biom15010020.

Abstract

Obesity leads to a chronic inflammatory state throughout the body, with increased infiltration of immune cells and inflammatory factors in skeletal muscle tissue, and, at the same time, the level of intracellular mitochondrial oxidative stress rises. Meanwhile, obesity is closely related to the development of skeletal muscle fibrosis and can affect the metabolic function of skeletal muscle, triggering metabolic disorders such as insulin resistance (IR) and type 2 diabetes (T2D). However, whether there is a mutual regulatory effect between the two pathological states of inflammation and fibrosis in obese skeletal muscle and the specific molecular mechanisms have not been fully clarified. This review focuses on the pathological changes of skeletal muscle inflammation and fibrosis induced by obesity, covering the metabolic changes it causes, such as lipid deposition, mitochondrial dysfunction, and dysregulation of inflammatory factors, aiming to reveal the intricate connections between the two. In terms of intervention strategies, aerobic exercise, dietary modification, and pharmacotherapy can improve skeletal muscle inflammation and fibrosis. This article provides insight into the important roles of inflammation and fibrosis in the treatment of obesity and the management of skeletal muscle diseases, aiming to provide new ideas for the diagnosis and treatment of metabolic diseases such as obesity and IR.

摘要

肥胖会导致全身慢性炎症状态,骨骼肌组织中免疫细胞和炎症因子的浸润增加,同时细胞内线粒体氧化应激水平升高。与此同时,肥胖与骨骼肌纤维化的发展密切相关,可影响骨骼肌的代谢功能,引发胰岛素抵抗(IR)和2型糖尿病(T2D)等代谢紊乱。然而,肥胖骨骼肌中炎症和纤维化这两种病理状态之间是否存在相互调节作用以及具体分子机制尚未完全阐明。本综述聚焦于肥胖引起的骨骼肌炎症和纤维化的病理变化,涵盖其导致的代谢变化,如脂质沉积、线粒体功能障碍和炎症因子失调,旨在揭示两者之间的复杂联系。在干预策略方面,有氧运动、饮食调整和药物治疗可改善骨骼肌炎症和纤维化。本文深入探讨了炎症和纤维化在肥胖治疗及骨骼肌疾病管理中的重要作用,旨在为肥胖和IR等代谢性疾病的诊断与治疗提供新思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82ee/11764331/68a35d9c958a/biomolecules-15-00020-g001.jpg

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