ArticleLife science alliance2024
STAT3 inhibition recovers regeneration of aged muscles by restoring autophagy in muscle stem cells.
Article in Life science alliance, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Review
- Transcriptional profiling of male mouse muscle across aging stages: a gene ontology analysis of the muscle matreotype.BMC genomics · 2026Article
- Enhancement of Hypoxia-Induced Autophagy via the HIF-1apha/BNIP3 Pathway Promotes Proliferation and Myogenic Differentiation of Aged Skeletal Muscle Satellite Cells.Life (Basel, Switzerland) · 2026Article
- Exercise-modulated IL-6 in cancer cachexia: molecular mechanisms and therapeutic potential.Journal of translational medicine · 2026Review
- Modulation of the JAK2-STAT3 pathway promotes expansion and maturation of human iPSC-derived myogenic progenitor cells.Stem cell reports · 2025Article
- Autophagy-senescence interplay in kidney disease: mechanistic insights and therapeutic potential.Molecular biology reports · 2025Review
- The transcription factor STAT3 and aging: an intermediate medium.Biogerontology · 2025Review
- Metabolic regulation in adult and aging skeletal muscle stem cells.Genes & development · 2025Review
- Unraveling the role of STAT3 in Cancer Cachexia: pathogenic mechanisms and therapeutic opportunities.Frontiers in endocrinology · 2025Review
- Autophagy in Muscle Regeneration: Mechanisms, Targets, and Therapeutic Perspective.International journal of molecular sciences · 2024Review
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Authors and funding
12 authors.
Funding
Abstract
Age-related reduction in muscle stem cell (MuSC) regenerative capacity is associated with cell-autonomous and non-cell-autonomous changes caused by alterations in systemic and skeletal muscle environments, ultimately leading to a decline in MuSC number and function. Previous studies demonstrated that STAT3 plays a key role in driving MuSC expansion and differentiation after injury-activated regeneration, by regulating autophagy in activated MuSCs. However, autophagy gradually declines in MuSCs during lifespan and contributes to the impairment of MuSC-mediated regeneration of aged muscles. Here, we show that STAT3 inhibition restores the autophagic process in aged MuSCs, thereby recovering MuSC ability to promote muscle regeneration in geriatric mice. We show that STAT3 inhibition could activate autophagy at the nuclear level, by promoting transcription of autophagy-related genes, and at the cytoplasmic level, by targeting STAT3/PKR phosphorylation of eIF2α. These results point to STAT3 inhibition as a potential intervention to reverse the age-related autophagic block that impairs MuSC ability to regenerate aged muscles. They also reveal that STAT3 regulates MuSC function by both transcription-dependent and transcription-independent regulation of autophagy.
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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.