ArticleStem cell reports2018
Loss of MyoD and Myf5 in Skeletal Muscle Stem Cells Results in Altered Myogenic Programming and Failed Regeneration.
Article in Stem cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 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
103 citing papers in PubMed, 159 citations in OpenAlex.
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- ASB5 is a specific marker for muscle satellite cells but dispensable for skeletal muscle development and regeneration.Skeletal muscle · 2026Article
- WDR62 is required for proper proliferation and early differentiation of skeletal myoblasts.Communications biology · 2026Article
- Skeletal muscle reprogramming in peripheral nerve injury: mechanisms, therapeutic roles, and complication management.Experimental biology and medicine (Maywood, N.J.) · 2026Review
- FTO promotes skeletal muscle differentiation and regeneration by regulating mbioRxiv : the preprint server for biology · 2025Article
- The role of muscle fascia in heterotopic ossification and maintenance of skeletal muscle integrity in fibrodysplasia ossificans progressiva.bioRxiv : the preprint server for biology · 2025Article
- MYOD represses gene expression from non-E-box motifs.Genes & development · 2025Article
- Hyaluronic Acid-Coated Melt Electrowritten Scaffolds Promote Myoblast Attachment, Alignment, and Differentiation.Cellular and molecular bioengineering · 2025Article
- X-Linked Hypophosphatemia: Role of Fibroblast Growth Factor 23 on Human Skeletal Muscle-Derived Cells.Calcified tissue international · 2025Article
- Hyaluronic Acid-Coated Melt Electrowritten Scaffolds Promote Myoblast Attachment, Alignment, and Differentiation.bioRxiv : the preprint server for biology · 2025Article
43 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MyoD and Myf5 are fundamental regulators of skeletal muscle lineage determination in the embryo, and their expression is induced in satellite cells following muscle injury. MyoD and Myf5 are also expressed by satellite cell precursors developmentally, although the relative contribution of historical and injury-induced expression to satellite cell function is unknown. We show that satellite cells lacking both MyoD and Myf5 (double knockout [dKO]) are maintained with aging in uninjured muscle. However, injured muscle fails to regenerate and dKO satellite cell progeny accumulate in damaged muscle but do not undergo muscle differentiation. dKO satellite cell progeny continue to express markers of myoblast identity, although their myogenic programming is labile, as demonstrated by dramatic morphological changes and increased propensity for non-myogenic differentiation. These data demonstrate an absolute requirement for either MyoD or Myf5 in muscle regeneration and indicate that their expression after injury stabilizes myogenic identity and confers the capacity for muscle differentiation.
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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 OpenQuestion graph.