ArticleiScience2025
The matricellular protein ADAMTS-like 2 regulates differentiation of skeletal muscle-resident fibro-adipogenic progenitor cells.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed.
- Phase-transition failure in aged skeletal muscle regeneration.Biogerontology · 2026Review
- 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
- Stimulation of EGFR signaling in fibro-adipogenic precursors decreases adipogenesis in Duchenne muscular dystrophy.Skeletal muscle · 2026Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Skeletal muscle development and regeneration requires the activities of myogenic and non-myogenic muscle stem cell populations. Non-myogenic muscle stem cells, such as fibro-adipogenic progenitors (FAPs), play important roles in muscle regeneration after injury. Activated FAPs promote myogenic muscle stem cell differentiation and contribute to the restoration of muscle architecture. In pathological conditions, FAPs can differentiate into adipocytes or fibroblasts, causing fatty infiltrations or muscle fibrosis, respectively. Here, we identified the extracellular matrix protein ADAMTS-like 2 (
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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.