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NLRP3炎性小体在肌肉减少症中的功能新见解:机制与治疗策略

New insights into the function of the NLRP3 inflammasome in sarcopenia: mechanism and therapeutic strategies.

作者信息

Zou Yunyi, Tang Xiangbin, Yang Siyuan, Chen Zhanglin, Liu Bin, Zhou Zuoqiong, Peng Xiyang, Tang Changfa

机构信息

State Key Laboratory of Developmental Biology of Freshwater Fish, Key Laboratory of Physical Fitness and Exercise Rehabilitation of Hunan Province, College of Physical Education, Hunan Normal University, Changsha, China.

State Key Laboratory of Developmental Biology of Freshwater Fish, Key Laboratory of Physical Fitness and Exercise Rehabilitation of Hunan Province, College of Physical Education, Hunan Normal University, Changsha, China.

出版信息

Metabolism. 2024 Sep;158:155972. doi: 10.1016/j.metabol.2024.155972. Epub 2024 Jul 6.

DOI:10.1016/j.metabol.2024.155972
PMID:38972476
Abstract

Sarcopenia is one of the most common skeletal muscle disorders and is characterized by infirmity and disability. While extensive research has focused on elucidating the mechanisms underlying the progression of sarcopenia, further comprehensive insights into its pathogenesis are necessary to identify new preventive and therapeutic approaches. The involvement of inflammasomes in sarcopenia is widely recognized, with particular emphasis on the NLRP3 (NLR family pyrin domain containing 3) inflammasome. In this review, we aim to elucidate the underlying mechanisms of the NLRP3 inflammasome and its relevance in sarcopenia of various etiologies. Furthermore, we highlight interventions targeting the NLRP3 inflammasome in the context of sarcopenia and discuss the current limitations of our knowledge in this area.

摘要

肌肉减少症是最常见的骨骼肌疾病之一,其特征是虚弱和残疾。虽然广泛的研究集中在阐明肌肉减少症进展的潜在机制,但有必要对其发病机制进行更全面的深入了解,以确定新的预防和治疗方法。炎性小体参与肌肉减少症已得到广泛认可,尤其强调NLRP3(含NLR家族pyrin结构域3)炎性小体。在本综述中,我们旨在阐明NLRP3炎性小体的潜在机制及其在各种病因的肌肉减少症中的相关性。此外,我们强调在肌肉减少症背景下针对NLRP3炎性小体的干预措施,并讨论我们在该领域现有知识的局限性。

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Front Pharmacol. 2025 Jun 30;16:1541373. doi: 10.3389/fphar.2025.1541373. eCollection 2025.
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Aging Clin Exp Res. 2024 Dec 27;37(1):13. doi: 10.1007/s40520-024-02903-7.