.png){kind=icon}
.png){kind=icon}
Return
TGF-β2 drives lipid droplet accumulation in chondrocytes through the TβRI/p-Smad3/Fabp5 axis
.png){kind=icon}
OA
AI
J
C
Y
W
J
X
DOI：10.1016/j.jbc.2026.113317.png)
.png){kind=icon}
.png){kind=icon}
Share.png){kind=icon}
Save
Abstract
En 中文
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.
Keywords:
Osteoarthritis
Chondrocyte
Lipid metabolism
Transforming growth factor-β2
AI Summary
Key information extracted from the uploaded paper, including a brief overview, abstract, background, key highlights, visual analysis, and future outlook.
Journal
IF:
3.9
Papers:
11.2W
Citations:
28.3W
Organization
Cited Papers