ArticleNature communications2025
Stage-specific and cell-autonomous functions of Delta-like 1 in skeletal muscle stem cells and myogenesis.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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Who cites it
5 citing papers in PubMed.
- KMT5A maintains muscle stem cell quiescence through epigenetic regulation of Notch signaling.iScience · 2026Article
- Mechanisms of Impaired Skeletal Muscle Regeneration and Therapeutic Approaches in Aging and Chronic Disease.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Regenerative Medicine: Advanced Therapy for Muscle Tissue Restoration.International journal of molecular sciences · 2026Review
- Single-Cell Sequencing Reveals the Crosstalk Between MuSCs and FAPs in Ruminant Skeletal Muscle Development.Cells · 2026Article
- Beyond hormone deficiency: a framework for endocrine-immune-niche integration in aging skeletal muscle regeneration.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
NOTCH signaling plays multiple roles in muscle satellite cells (MuSCs), but the regulation of NOTCH signaling in MuSCs is poorly defined. Using conditional knockout (cKO) mice, here we explore the role of Delta-Like 1 (DLL1), a ligand of NOTCH receptors, in MuSCs and myogenesis. Dll1-cKO in embryonic myoblasts, but not post-differentiation myocytes, diminishes myogenic progenitors and myogenesis. Dll1-cKO in MuSCs of adult mice disrupts MuSCs homeostasis in non-injured muscles, leading to precocious differentiation, self-renewal deficiency, and regenerative failure upon injuries. These defects of Dll1-cKO myoblasts are cell intrinsic, as they cannot be rescued by cocultured wild-type myoblasts. Overexpression of full-length Dll1 leads to a truncated intracellular domain (DLL1ICD), which promotes differentiation and fusion of myoblasts. Thus, besides its widely accepted role in transactivating NOTCH in a neighboring cell, DLL1ICD also plays a cell-autonomous role in the Dll1-expressing cell. These cell-autonomous and non-autonomous roles together are essential for embryonic myogenesis and postnatal regeneration.
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Registered trials
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