ArticleThe Journal of biological chemistry2026
TGF-β2 drives lipid droplet accumulation in chondrocytes through the TβRI/p-smad3/fabp5 axis.
Article in The Journal of biological chemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Chondrocytes preserve cartilage lipid homeostasis by storing neutral lipids in lipid droplets and controlling their turnover through coordinated biochemical signaling. TGF-β2 is elevated in osteoarthritis and regulates key chondrocyte functions, including proliferation, differentiation, and cell death. However, whether and how TGF-β2 regulates chondrocyte lipid metabolism remains unknown. Here, we characterize TGF-β2-regulated lipid droplet accumulation and delineate the underlying mechanism. TGF-β2 drives neutral lipid and lipid droplet accumulation in chondrocytes and cartilage through upregulation of Fabp5. This effect requires TGF-β2 signaling through receptor TβRI, which induces the phosphorylation and nuclear translocation of Smad3, thereby promoting Fabp5 transcription. In this process, TGF-β2 induces enrichment of cellular lipid intermediates involved in lipid droplet accumulation. Collectively, our findings reveal a novel TGF-β2/TβRI/p-Smad3/Fabp5 signaling axis that regulates lipid storage in chondrocytes and suggest potential metabolic targets for maintaining cartilage homeostasis and treating related diseases.
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