ArticleNature communications2026
Sarcopenia promotes tumorigenesis by disrupting NOTCH-SDC2-regulated biogenesis of muscle-derived extracellular vesicles.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- The Impact of Ageing on Skeletal Muscle: Roles of Mitochondrial Dysregulation, Systemic Communication, and Exercise.Journal of cellular physiology · 2026Review
- Isolation and Biophysical Characterization of Extracellular Vesicles Released by Myocytes.Bio-protocol · 2026Article
- Inflammaging and osteoarthritis - therapeutic opportunities.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Sarcopenia is an age-related condition characterized by loss of skeletal muscle mass and strength and is associated with increased cancer incidence and mortality, yet how muscle decline promotes tumorigenesis remains unclear. Here, we show that skeletal muscle functions as an anti-tumor organ by secreting extracellular vesicles (EVs) that suppress tumor growth. Using Drosophila melanogaster and mouse cancer models, we demonstrate that muscle-derived EVs inhibit tumorigenesis. In contrast, sarcopenic muscle exhibits reduced EV secretion and altered EV cargo, resulting in loss of tumor-suppressive activity. We identify miR-7a-5p as a tumor-suppressive microRNA enriched in EVs from healthy muscle but diminished with aging, where it restrains tumor growth by inhibiting TEAD1 signaling. Mechanistically, muscle EV biogenesis is regulated by a NOTCH-SDC2 pathway that declines with age but is reactivated by exercise. Together, these findings define a muscle-to-tumor communication axis with therapeutic potential.
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