Fat infiltration in skeletal muscle: Influential triggers and regulatory mechanism.
| Autor: | Wang L; College of Animal Sciences, Zhejiang University, Hangzhou, China.; Key Laboratory of Molecular Animal Nutrition (Zhejiang University), Ministry of Education, Hangzhou, China.; Key Laboratory of Animal Feed and Nutrition of Zhejiang Province, Hangzhou, China., Valencak TG; College of Animal Sciences, Zhejiang University, Hangzhou, China., Shan T; College of Animal Sciences, Zhejiang University, Hangzhou, China.; Key Laboratory of Molecular Animal Nutrition (Zhejiang University), Ministry of Education, Hangzhou, China.; Key Laboratory of Animal Feed and Nutrition of Zhejiang Province, Hangzhou, China. |
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| Jazyk: | angličtina |
| Zdroj: | IScience [iScience] 2024 Feb 15; Vol. 27 (3), pp. 109221. Date of Electronic Publication: 2024 Feb 15 (Print Publication: 2024). |
| DOI: | 10.1016/j.isci.2024.109221 |
| Abstrakt: | Fat infiltration in skeletal muscle (also known as myosteatosis) is now recognized as a distinct disease from sarcopenia and is directly related to declining muscle capacity. Hence, understanding the origins and regulatory mechanisms of fat infiltration is vital for maintaining skeletal muscle development and improving human health. In this article, we summarized the triggering factors such as aging, metabolic diseases and metabolic syndromes, nonmetabolic diseases, and muscle injury that all induce fat infiltration in skeletal muscle. We discussed recent advances on the cellular origins of fat infiltration and found several cell types including myogenic cells and non-myogenic cells that contribute to myosteatosis. Furthermore, we reviewed the molecular regulatory mechanism, detection methods, and intervention strategies of fat infiltration in skeletal muscle. Based on the current findings, our review will provide new insight into regulating function and lipid metabolism of skeletal muscle and treating muscle-related diseases. Competing Interests: The authors declare no conflict of interest. (© 2024 The Authors.) |
| Databáze: | MEDLINE |
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