ArticleiScience2025
SESN2 maintains cartilage homeostasis by SREBP1-mediated lipid metabolism during osteoarthritis progression.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
2 citing papers in PubMed.
- Multi‑omics integration in osteoarthritis: Unraveling cell‑type‑specific gene‑metabolite networks for precision medicine (Review).International journal of molecular medicine · 2026Review
- Integrating network pharmacology, microbiomics, and metabolomics to uncover the therapeutic effect of Liubao tea on osteoarthritis.Frontiers in immunology · 2026Article
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Authors and funding
15 authors.
Funding
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Abstract
Chondrocytes experience adverse lipid metabolism disorders during the degeneration of cartilage in osteoarthritis (OA), while the underlying mechanisms remain poorly understood. Sestrin2 (SESN2), a highly conserved stress-inducible protein, plays a crucial role in regulating lipid metabolism. This study aimed to investigate the role of SESN2 in the regulation of fatty acid metabolism in chondrocytes and elucidate the underlying molecular mechanisms in OA. The expression of SESN2 was significantly decreased in OA-affected human cartilage, and this decrease correlated with the upregulation of lipogenic enzymes. Sesn2 inhibited lipogenic enzyme expression in chondrocytes and improved cartilage homeostasis. Mechanistically, SESN2 inhibited the expression of sterol regulatory element-binding transcription factor 1 (SREBP1) and interacted with SREBP cleavage-activating protein (SCAP) to deactivate SREBP1-mediated transcription for lipogenesis. Finally, overexpression of
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