ArticleEMBO reports2025
Immune aging impairs muscle regeneration via macrophage-derived anti-oxidant selenoprotein P.
Article in EMBO reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Review
- Selenium Deficiency is a Significant Risk Factor for Sarcopenia: Evidence and Selenoprotein-Mediated Mechanisms.Biological trace element research · 2026Review
- Phase-transition failure in aged skeletal muscle regeneration.Biogerontology · 2026Review
- The Impact of Ageing on Skeletal Muscle: Roles of Mitochondrial Dysregulation, Systemic Communication, and Exercise.Journal of cellular physiology · 2026Review
- Selenoprotein P deficiency in MASLD: association with insulin resistance and liver fibrosis: a prospective case-control study.BMC gastroenterology · 2026Article
- Pareto optimality reveals an atlas of cellular archetypes.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Beyond hormone deficiency: a framework for endocrine-immune-niche integration in aging skeletal muscle regeneration.Frontiers in immunology · 2026Review
- Identification and clinical evaluation of diagnostic biomarkers for ischemic cardiomyopathy based on machine learning and transcriptomics.Frontiers in cardiovascular medicine · 2026Article
- Skeletal muscle as a dynamic immunological niche for vaccination.Frontiers in immunology · 2026Review
- Immunosenescence as a driver of the transition from frailty to multimorbidity.Frontiers in immunology · 2026Review
- Regenerate to "Rejuvenate": Insights From Adult Resident Stem Cells of Aged Flatworms and Mice.Aging cell · 2025Review
- Molecular Framework of the Onset and Progression of Skeletal Muscle Aging.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Muscle regeneration is impaired with aging, due to both intrinsic defects of muscle stem cells (MuSCs) and alterations of their niche. Here, we monitor the cells constituting the MuSC niche over time in young and old regenerating mouse muscle. Aging alters the expansion of all niche cells, with prominent phenotypes in macrophages that show impaired resolution of inflammation. RNA sequencing of FACS-isolated mononucleated cells uncovers specific profiles and kinetics of genes and molecular pathways in old versus young muscle cells, indicating that each cell type responds to aging in a specific manner. Moreover, we show that macrophages have an altered expression of Selenoprotein P (Sepp1). Macrophage-specific deletion of Sepp1 is sufficient to impair the acquisition of their restorative profile and causes inefficient skeletal muscle regeneration. When transplanted in aged mice, bone marrow from young WT mice, but not Sepp1-KOs, restores muscle regeneration. This work provides a unique resource to study MuSC niche aging, reveals that niche cell aging is asynchronous and establishes the antioxidant Selenoprotein P as a driver of age-related decline of muscle regeneration.
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Registered trials
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