ArticleeLife2016
Myofiber-specific TEAD1 overexpression drives satellite cell hyperplasia and counters pathological effects of dystrophin deficiency.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 19 citations in OpenAlex.
- FGFR1 and FGFR4 are essential regulators of muscle stem cell quiescence.Cell communication and signaling : CCS · 2025Article
- Autophagy in adult stem cell homeostasis, aging, and disease therapy.Cell regeneration (London, England) · 2025Review
- Methylome-proteome integration after late-life voluntary exercise training reveals regulation and target information for improved skeletal muscle health.The Journal of physiology · 2025Article
- Inhibition of MAT2A Impairs Skeletal Muscle Repair Function.Biomolecules · 2024Article
- Dynamic alternations of three-dimensional chromatin architecture contribute to phenotypic characteristics of breast muscle in chicken.Communications biology · 2024Article
- Effect of TEA domain transcription factor 1 (Animal biotechnology · 2023Article
- Multi-Omics Analysis Reveals the Potential Effects of Maternal Dietary Restriction on Fetal Muscle Growth and Development.Nutrients · 2023Article
- Article
- A Tead1-Apelin axis directs paracrine communication from myogenic to endothelial cells in skeletal muscle.iScience · 2022Article
- Fibroblast growth factor 6 regulates sizing of the muscle stem cell pool.Stem cell reports · 2021Article
- Translational research on Myology and Mobility Medicine: 2021 semi-virtual PDM3 from Thermae of Euganean Hills, May 26 - 29, 2021.European journal of translational myology · 2021Article
- Muscle progenitor specification and myogenic differentiation are associated with changes in chromatin topology.Nature communications · 2020Article
- Inhibition of microRNA-92a increases blood vessels and satellite cells in skeletal muscle but does not improve duchenne muscular dystrophy-related phenotype in mdx mice.Muscle & nerve · 2019Article
- Starring or Supporting Role? Satellite Cells and Skeletal Muscle Fiber Size Regulation.Physiology (Bethesda, Md.) · 2018Review
- Skeletal muscle stem cells in comfort and stress.NPJ Regenerative medicine · 2018Review
- Depletion of Pax7+ satellite cells does not affect diaphragm adaptations to running in young or aged mice.The Journal of physiology · 2017Article
- Vestigial-like 2 contributes to normal muscle fiber type distribution in mice.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
When unperturbed, somatic stem cells are poised to affect immediate tissue restoration upon trauma. Yet, little is known regarding the mechanistic basis controlling initial and homeostatic 'scaling' of stem cell pool sizes relative to their target tissues for effective regeneration. Here, we show that TEAD1-expressing skeletal muscle of transgenic mice features a dramatic hyperplasia of muscle stem cells (i.e. satellite cells, SCs) but surprisingly without affecting muscle tissue size. Super-numeral SCs attain a 'normal' quiescent state, accelerate regeneration, and maintain regenerative capacity over several injury-induced regeneration bouts. In dystrophic muscle, the TEAD1 transgene also ameliorated the pathology. We further demonstrate that hyperplastic SCs accumulate non-cell-autonomously via signal(s) from the TEAD1-expressing myofiber, suggesting that myofiber-specific TEAD1 overexpression activates a physiological signaling pathway(s) that determines initial and homeostatic SC pool size. We propose that TEAD1 and its downstream effectors are medically relevant targets for enhancing muscle regeneration and ameliorating muscle pathology.
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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 OpenQuestion graph.