ArticleCell reports2021
Persistent NF-κB activation in muscle stem cells induces proliferation-independent telomere shortening.
Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The trial behind it
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Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- Preserved satellite cell pool in a laminin-α2-deficient model of congenital muscular dystrophy.Disease models & mechanisms · 2026Article
- Lifelong congenital untreated isolated GH deficiency does not alter human leukocyte telomere length.Journal of endocrinological investigation · 2026Article
- TRF2 couples muscle stem cell identity to regenerative repair.Science advances · 2026Article
- Aging and cancer: current understandings and future perspectives.Signal transduction and targeted therapy · 2026Review
- Inflammaging and Sarcopenia as Interconnected Hallmarks of Aging: Integrative Roles of Bioactive Compounds and Lifestyle Interventions.Nutrients · 2026Review
- TWEAK-induced alternative NF-κB signaling regulates Cxcl10 and Mymx to promote myoblast-to-myotube fusion and muscle regeneration.Communications biology · 2026Article
- Augmentation of DNA exonuclease TREX1 in macrophages as a therapy for cardiac ischemic injury.Science translational medicine · 2025Article
- Loss of cell-autonomously secreted laminin-α2 drives muscle stem cell dysfunction in LAMA2-related muscular dystrophy.Nature communications · 2025Article
- First Direct Evidence of Accelerated Molecular Aging in Intracranial Aneurysmal Tissue.Aging cell · 2025Article
- Frailty in lung transplant recipients is associated with anemia and telomere dysfunction but independent of epigenetic age.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2025Article
- Colchicine prevents oxidative stress-induced endothelial cell senescence via blocking NF-κB and MAPKs: implications in vascular diseases.Journal of inflammation (London, England) · 2023Article
- Genome-wide epigenetic dynamics during postnatal skeletal muscle growth in Hu sheep.Communications biology · 2023Article
- Impacts of radiation exposure, hindlimb unloading, and recovery on murine skeletal muscle cell telomere length.NPJ microgravity · 2023Article
- Chronic inflammation and the hallmarks of aging.Molecular metabolism · 2023Review
- Impaired muscle stem cell function and abnormal myogenesis in acquired myopathies.Bioscience reports · 2023Review
- Doxycycline Attenuated Ethanol-Induced Inflammaging in Endothelial Cells: Implications in Alcohol-Mediated Vascular Diseases.Antioxidants (Basel, Switzerland) · 2022Article
- Association between COVID-19 and telomere length: A bidirectional Mendelian randomization study.Journal of medical virology · 2022Article
- Tissue-specific Grb10/Ddc insulator drives allelic architecture for cardiac development.Molecular cell · 2022Article
- Piezo1 regulates the regenerative capacity of skeletal muscles via orchestration of stem cell morphological states.Science advances · 2022Article
- Systems approaches to investigate the role of NF-κB signaling in aging.The Biochemical journal · 2022Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
During the repeated cycles of damage and repair in many muscle disorders, including Duchenne muscular dystrophy (DMD), the muscle stem cell (MuSC) pool becomes less efficient at responding to and repairing damage. The underlying mechanism of such stem cell dysfunction is not fully known. Here, we demonstrate that the distinct early telomere shortening of diseased MuSCs in both mice and young DMD patients is associated with aberrant NF-κB activation. We find that prolonged NF-κB activation in MuSCs in chronic injuries leads to shortened telomeres and Ku80 dysregulation and results in severe skeletal muscle defects. Our studies provide evidence of a role for NF-κB in regulating stem-cell-specific telomere length, independently of cell replication, and could be a congruent mechanism that is applicable to additional tissues and/or diseases characterized by systemic chronic inflammation.
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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.