Open Access
Review
Asymmetric Cell Division and Satellite Cell Fate Regulation in Skeletal Muscle Aging and Disease
Shenghe Wang1, 2
, Guangchuang Yu3
, Liwei Xie1, 4, 5, *
Author Information
Submitted: 29 Jul 2024 | Revised: 30 Sept 2024 | Accepted: 20 Oct 2024 | Published: 30 Oct 2024
Abstract
Satellite cells, the resident muscle stem cells, play a crucial role in skeletal muscle regeneration, growth, and repair. Asymmetric cell division is a critical process regulating satellite cell self-renewal and differentiation, and is governed by various intrinsic and extrinsic factors. Key biomarkers of satellite cell characteristics, such as Pax7, MRFs, and Sprouty1, are essential in maintaining satellite cell homeostasis. Signaling pathways, including Notch, Wnt, TGF-β, FGF2, and the PAR complex, intricately regulate satellite cell division and fate determination. Asymmetric division is orchestrated through the establishment of cell polarity and differential distribution of fate determinants. Aging and diseases like Duchenne muscular dystrophy disrupt asymmetric division, leading to impaired satellite cell function and muscle regeneration. Potential therapeutic strategies aim to rejuvenate satellite cells and promote muscle regeneration by targeting the gut microbiome, utilizing gene editing technologies, and harnessing the power of exercise-induced factors. Understanding the molecular mechanisms governing satellite cell behavior and Keywords should be in lowercase and separated by semicolons. Developing innovative therapies hold promise for combating age-related muscle deterioration and pathological conditions characterized due to impaired muscle regeneration. Future research should focus on unraveling the complex regulatory networks and translating findings into effective clinical applications to restore muscle function.
Graphical Abstract
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Volume 1, Issue 1How to Cite
Wang, S., Yu, G., & Xie, L. (2024). Asymmetric Cell Division and Satellite Cell Fate Regulation in Skeletal Muscle Aging and Disease. Health and Metabolism, 1(1), 5. https://doi.org/10.53941/hm.2024.100005
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