AI Article Synopsis
- - Muscle regeneration after minor injuries relies on activating satellite cells (muscle stem cells) that differentiate into myoblasts and eventually myofibers.
- - The study identified ADAMTSL2 as an important protein that promotes the differentiation of myoblasts, influencing muscle development and regeneration.
- - The absence of ADAMTSL2 slows down muscle recovery after injury, while its introduction speeds up myoblast formation, suggesting its potential for therapeutic use in muscle repair.
Article Abstract
Skeletal muscle regeneration and functional recovery after minor injuries requires the activation of muscle-resident myogenic muscle stem cells (i.e. satellite cells) and their subsequent differentiation into myoblasts, myocytes, and ultimately myofibers. We recently identified secreted ADAMTS-like 2 (ADAMTSL2) as a pro-myogenic regulator of muscle development, where it promoted myoblast differentiation. Since myoblast differentiation is a key process in skeletal muscle regeneration, we here examined the role of ADAMTSL2 during muscle regeneration after BaCl injury. Specifically, we found that muscle regeneration was delayed after ablation of ADAMTSL2 in myogenic precursor cells and accelerated following injection of pro-myogenic ADAMTSL2 protein domains. Mechanistically, ADAMTSL2 regulated the number of committed myoblasts, which are the precursors for myocytes and regenerating myofibers. Collectively, our data support a role for myoblast-derived ADAMTSL2 as a positive regulator of muscle regeneration and provide a proof-of-concept for potential therapeutic applications.
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Source |
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| http://dx.doi.org/10.1038/s41536-024-00383-x | DOI Listing |
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11659564 | PMC |
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