Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2023 Aug 1;14:1230174. doi: 10.3389/fphar.2023.1230174

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2023 Yan, Zhou, Meng, Zhou, Jia, Li, Cui, Yu, Tang, Li, Zhang, Wang, Hou and Yang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

CD36 promotes pathologic synovial fibroblast-induced fibrosis in FS through the PI3k-Akt pathway. (A) The expression of p-Akt/Akt, as well as several key molecules in other classic fibrosis-related pathways including the TGF-β1/SMAD pathway and the WNT/β-catenin pathway, was examined in synovial fibroblasts treated with siRNA or SaB. (B,C) Western blotting and qRT-PCR results showed that COL 1, COL 3, FN and α-SMA along with Akt phosphorylation was significantly upregulated in FS synovial fibroblasts after the overexpression of CD36, and this trend was reversed by Akt inhibitor, MK2206. (D,E) Cell adhesion test and Wound-healing suggested that MK2206 inhibited the enhanced fibrosis-related functions in synovial fibroblasts caused by the overexpression of CD36. Scale bar: 50 μm *p < 0.05; **p < 0.01; ***p < 0.001.