ArticleMolecular and cellular biology2012
O(2) regulates skeletal muscle progenitor differentiation through phosphatidylinositol 3-kinase/AKT signaling.
Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.
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Who cites it
41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 70 citations in OpenAlex.
- Hypoxic Signaling in Skeletal Muscle Maintenance and Regeneration: A Systematic Review.Frontiers in physiology · 2021Pooled it
- A systematic review of p53 regulation of oxidative stress in skeletal muscle.Redox report : communications in free radical research · 2018Pooled it
- Effect of hyperbaric oxygen therapy on postoperative muscle damage and inflammation following total knee arthroplasty: a randomized controlled trial.Scientific reports · 2025Trial
- Role of Hypoxia-Inducible Factor-1α in Regulating Muscle Degeneration After Rotator Cuff Tears.The American journal of sports medicine · 2026Article
- Mild hyperbaric oxygen enhanced the regeneration of the tibialis anterior muscle after the cardiotoxin-induced muscle injury.Biochemistry and biophysics reports · 2026Article
- Transient hypoxia followed by progressive reoxygenation is required for muscle repair.EMBO reports · 2026Article
- Macrophage metabolic rewiring rejuvenates muscle Raman signatures and cellular remodeling during regrowth in aged mice.JCI insight · 2025Article
- Hypoxia and Tissue Regeneration: Adaptive Mechanisms and Therapeutic Opportunities.International journal of molecular sciences · 2025Review
- Directing cellular responses in a nanocomposite 3D matrix for tissue regeneration with nanoparticle-mediated drug delivery.Materials today. Bio · 2023Article
- Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting.International journal of molecular sciences · 2023Review
- Adaptive exhaustion during prolonged intermittent hypoxia causes dysregulated skeletal muscle protein homeostasis.The Journal of physiology · 2023Article
- The effect of hypoxia on myogenic differentiation and multipotency of the skeletal muscle-derived stem cells in mice.Stem cell research & therapy · 2022Article
- Hypoxia and Hypoxia-Inducible Factor Signaling in Muscular Dystrophies: Cause and Consequences.International journal of molecular sciences · 2021Review
- A Two-Week Insulin Infusion in Intrauterine Growth Restricted Fetal Sheep at 75% Gestation Increases Skeletal Myoblast Replication but Did Not Restore Muscle Mass or Increase Fiber Number.Frontiers in endocrinology · 2021Article
- An NRF2 Perspective on Stem Cells and Ageing.Frontiers in aging · 2021Review
- HIF-hypoxia signaling in skeletal muscle physiology and fibrosis.Journal of cell communication and signaling · 2020Review
- Increase in HDAC9 suppresses myoblast differentiation via epigenetic regulation of autophagy in hypoxia.Cell death & disease · 2019Article
- Assessment of different strategies for scalable production and proliferation of human myoblasts.Cell proliferation · 2019Article
- Histone demethylase KDM6A directly senses oxygen to control chromatin and cell fate.Science (New York, N.Y.) · 2019Article
- Transient HIF2A inhibition promotes satellite cell proliferation and muscle regeneration.The Journal of clinical investigation · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Skeletal muscle stem/progenitor cells, which give rise to terminally differentiated muscle, represent potential therapies for skeletal muscle diseases. Delineating the factors regulating these precursors will facilitate their reliable application in human muscle repair. During embryonic development and adult regeneration, skeletal muscle progenitors reside in low-O(2) environments before local blood vessels and differentiated muscle form. Prior studies established that low O(2) levels (hypoxia) maintained muscle progenitors in an undifferentiated state in vitro, although it remained unclear if progenitor differentiation was coordinated with O(2) availability in vivo. In addition, the molecular signals linking O(2) to progenitor differentiation are incompletely understood. Here we show that the muscle differentiation program is repressed by hypoxia in vitro and ischemia in vivo. Surprisingly, hypoxia can significantly impair differentiation in the absence of hypoxia-inducible factors (HIFs), the primary developmental effectors of O(2). In order to maintain the undifferentiated state, low O(2) levels block the phosphatidylinositol 3-kinase/AKT pathway in a predominantly HIF1α-independent fashion. O(2) deprivation affects AKT activity by reducing insulin-like growth factor I receptor sensitivity to growth factors. We conclude that AKT represents a key molecular link between O(2) and skeletal muscle differentiation.
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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.