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RESEARCH PAPER / 2024-11-27

Autophagy in Muscle Regeneration: Mechanisms, Targets, and Therapeutic Perspective.

Yun Chu, Xinrun Yuan, Yiming Tao, Bin Yang, Jinlong Luo

Department of Intensive Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. · pubmed

Abstract

Autophagy maintains the stability of eukaryotic cells by degrading unwanted components and recycling nutrients and plays a pivotal role in muscle regeneration by regulating the quiescence, activation, and differentiation of satellite cells. Effective muscle regeneration is vital for maintaining muscle health and homeostasis. However, under certain disease conditions, such as aging, muscle regeneration can fail due to dysfunctional satellite cells. Dysregulated autophagy may limit satellite cell self-renewal, hinder differentiation, and increase susceptibility to apoptosis, thereby impeding muscle regeneration. This review explores the critical role of autophagy in muscle regeneration, emphasizing its interplay with apoptosis and recent advances in autophagy research related to diseases characterized by impaired muscle regeneration. Additionally, we discuss new approaches involving autophagy regulation to promote macrophage polarization, enhancing muscle regeneration. We suggest that utilizing cell therapy and biomaterials to modulate autophagy could be a promising strategy for supporting muscle regeneration. We hope that this review will provide new insights into the treatment of muscle diseases and promote muscle regeneration.

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper discusses the role of autophagy in muscle regeneration, particularly in the context of aging and the dysfunction of satellite cells, which is relevant to longevity research. However, while it presents solid insights into the mechanisms of muscle regeneration and potential therapeutic approaches, it does not propose a novel solution to the root causes of aging itself. Thus, its impact is solid but limited, making it a valuable contribution without being groundbreaking.

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