ArticleAging cell2026
Exosome-Delivered eNAMPT From Exercise Activates SIRT1 to Counteract Age-Related Hepatic Steatosis and Fibrosis.
Article in Aging cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Metabolic dysfunction-associated steatotic liver disease: pathogenic mechanisms and exercise-induced molecular adaptations.Lipids in health and disease · 2026Review
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Authors and funding
10 authors.
Funding
Abstract
Aging is a major independent risk factor for the development and progression of metabolic dysfunction-associated steatotic liver disease (MASLD); however, effective therapeutic strategies for this population remain limited. Here, we established a model of aging-associated MASLD by subjecting aged mice to a long-term high-fat diet (HFD), which recapitulated key disease features including progressive hepatic steatosis, inflammation, insulin resistance, and fibrosis. A 6-week exercise intervention markedly ameliorated these pathologies by restoring insulin sensitivity and suppressing TGF-β/Smad-mediated fibrotic signaling. We identified exercise-derived exosomes (Exercise-Exos) as primary mediators of these benefits. Western blot analysis revealed that extracellular nicotinamide phosphoribosyltransferase (eNAMPT) was markedly enriched in Exercise-Exos compared to those from sedentary controls. Delivery of exosomal eNAMPT activated the hepatic SIRT1-autophagy axis, restored autophagic flux, and inhibited epithelial-mesenchymal transition (EMT). These effects were demonstrated by an increased LC3-II/LC3-I ratio, reduced p62 accumulation, downregulation of mesenchymal markers (α-SMA, Vimentin), and upregulation of the epithelial marker E-cadherin. Furthermore, Exercise-Exos treatment significantly reduced collagen deposition. Critically, all protective effects were abolished upon pharmacological inhibition of SIRT1 with EX-527, establishing the necessity of the eNAMPT-NAD
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