ArticleThe EMBO journal2019
YY1 regulates skeletal muscle regeneration through controlling metabolic reprogramming of satellite cells.
Article in The EMBO journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed, 108 citations in OpenAlex.
- Identification of Enhancers and Transcription Factors Regulating Postnatal Growth of Skeletal Muscle in Cattle.Biology · 2026Article
- YY1 in hematopoietic stem cells: epigenetic regulation, chromatin architecture, and aging.Current opinion in hematology · 2026Review
- The use of molecular cues to regenerate musculoskeletal tissues.Innovative surgical sciences · 2026Review
- Current Progress in the Role of Ferroptosis in Skeletal Muscle Atrophy.Mediators of inflammation · 2026Review
- Adenosine Triggers an ADK-Dependent Intracellular Signaling Pathway Interacts PFKFB3-Mediated Glycolytic Metabolism to Promote Newly Formed Myofibers Development.International journal of molecular sciences · 2025Article
- Non-canonical roles of Keap1/Nrf2 in regulating quiescence and early activation in adult muscle stem cells.Nature communications · 2025Article
- Microglia-Derived Extracellular Vesicles Enhance Oligodendrocyte Maturation by Transcriptionally Regulating Mitochondrial Molecular Pathways.Cellular and molecular neurobiology · 2025Article
- Transcription factor Yin-Yang 1 governs cardiac metabolic reprogramming in response to exercise or pathological stress.American journal of physiology. Heart and circulatory physiology · 2025Article
- Perspectives on mitochondrial dysfunction in the regeneration of aging skeletal muscle.Cellular & molecular biology letters · 2025Review
- Multiomics and cellular senescence profiling of aging human skeletal muscle uncovers Maraviroc as a senotherapeutic approach for sarcopenia.Nature communications · 2025Article
- Skeletal muscle-specific Bambi deletion induces hypertrophy and oxidative switching coupling with adipocyte thermogenesis against metabolic disorders.Science China. Life sciences · 2025Article
- Iron homeostasis and ferroptosis in muscle diseases and disorders: mechanisms and therapeutic prospects.Bone research · 2025Review
- Metabolic regulation in adult and aging skeletal muscle stem cells.Genes & development · 2025Review
- Skeletal muscle stem cells modulate niche function in Duchenne muscular dystrophy mouse through YY1-CCL5 axis.Nature communications · 2025Article
- Pervasive RNA-binding protein enrichment on TAD boundaries regulates TAD organization.Nucleic acids research · 2025Article
- Integrative genetic and epigenetic control of skeletal muscle fiber traits in agricultural animals.Frontiers in genetics · 2025Review
- Unraveling the RKIP-YY1 axis: immune crosstalk in the pathogenesis of metabolic disorders.Frontiers in immunology · 2025Review
- PathoEye: A deep learning framework for the whole-slide image analysis of skin tissue.Computational and structural biotechnology journal · 2025Article
- Study on the pathogenesis of varicocele induced by the ferroptosis of cremaster satellite cells with the m6A modification of TFRC mRNA.PloS one · 2025Article
- Article
11 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Skeletal muscle satellite cells (SCs) are adult muscle stem cells responsible for muscle regeneration after acute or chronic injuries. The lineage progression of quiescent SC toward activation, proliferation, and differentiation during the regeneration is orchestrated by cascades of transcription factors (TFs). Here, we elucidate the function of TF Yin Yang1 (YY1) in muscle regeneration. Muscle-specific deletion of YY1 in embryonic muscle progenitors leads to severe deformity of diaphragm muscle formation, thus neonatal death. Inducible deletion of YY1 in SC almost completely blocks the acute damage-induced muscle repair and exacerbates the chronic injury-induced dystrophic phenotype. Examination of SC revealed that YY1 loss results in cell-autonomous defect in activation and proliferation. Mechanistic search revealed that YY1 binds and represses mitochondrial gene expression. Simultaneously, it also stabilizes Hif1α protein and activates Hif1α-mediated glycolytic genes to facilitate a metabolic reprogramming toward glycolysis which is needed for SC proliferation. Altogether, our findings have identified YY1 as a key regulator of SC metabolic reprogramming through its dual roles in modulating both mitochondrial and glycolytic pathways.
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