ArticleMatrix biology : journal of the International Society for Matrix Biology2023
Secreted ADAMTS-like 2 promotes myoblast differentiation by potentiating WNT signaling.
Article in Matrix biology : journal of the International Society for Matrix Biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Losartan shows limited benefit in preclinical models of Geleophysic dysplasia.Scientific reports · 2026Article
- The Pathogenic ADAMTSL2 D167N Variant Causes Geleophysic Dysplasia-Like Connective Tissue Changes in Mice.The American journal of pathology · 2026Article
- The matricellular protein ADAMTS-like 2 regulates differentiation of skeletal muscle-resident fibro-adipogenic progenitor cells.iScience · 2025Article
- ADAMTS4 Reduction Contributes to Extracellular Matrix Deposition and Impaired Myogenesis in the Skeletal Muscle of Cigarette Smoke-Exposed Mice.Biomedicines · 2025Article
- Myoblast-derived ADAMTS-like 2 promotes skeletal muscle regeneration after injury.NPJ Regenerative medicine · 2024Article
- The maternal lifestyle in pregnancy: Implications for foetal skeletal muscle development.Journal of cachexia, sarcopenia and muscle · 2024Review
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Myogenesis is the process that generates multinucleated contractile myofibers from muscle stem cells during skeletal muscle development and regeneration. Myogenesis is governed by myogenic regulatory transcription factors, including MYOD1. Here, we identified the secreted matricellular protein ADAMTS-like 2 (ADAMTSL2) as part of a Wnt-dependent positive feedback loop, which augmented or sustained MYOD1 expression and thus promoted myoblast differentiation. ADAMTSL2 depletion resulted in severe retardation of myoblast differentiation in vitro and its ablation in myogenic precursor cells resulted in aberrant skeletal muscle architecture. Mechanistically, ADAMTSL2 potentiated WNT signaling by binding to WNT ligands and WNT receptors. We identified the WNT-binding ADAMTSL2 peptide, which was sufficient to promote myogenesis in vitro. Since ADAMTSL2 was previously described as a negative regulator of TGFβ signaling in fibroblasts, ADAMTSL2 now emerges as a signaling hub that could integrate WNT, TGFβ and potentially other signaling pathways within the dynamic microenvironment of differentiating myoblasts during skeletal muscle development and regeneration.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.