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. 2021 May 28;9:664168. doi: 10.3389/fcell.2021.664168

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Copyright © 2021 Chen, Tan, Hu, Liu, Peng, Li and Wu.

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.

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The TGF-β and BMP signaling pathway in chondrocytes. When TGF-β or BMPs bind to type II receptor, type I receptor is transphosphorylated, which activate Smad-dependent signaling or non-Smad-dependent signaling (MAPK signaling). In the Smad-dependent signaling, R-Smads (the TGF-β-specific R-Smads is Smad2, 3 and the BMP-specific R-Smads is Smad1, 5, 8) are phosphorylated, and then it forms complexes with Co-Smad (Smad4). Next the complexes transfer into nucleus to regulate the expression of Sox9 and Runx2. MAPK signaling can phosphorylate Runx2 to increase its transcription activity, and it also can activate JNK and p38 kinases to change the balance between Smad2/3 and Smad1/5/8.