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. 2023 Jan 2;11:2. doi: 10.1038/s41413-022-00239-4

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — Schematic diagram showing the transforming growth factor-beta 3 (TGF-β3)-mediated R-Smad-dependent signaling pathway. Smad proteins transduce signals from the cell membrane to the nucleus and regulate gene expression after TGF-β3 binding to a TGF-β receptor (TβR). TGF-β3 plays a dual role in articular cartilage. It is involved in cartilaginous homeostasis via the classical Smad2/3 pathway and chondrocyte hypertrophy via the Smad1/5/8 pathway. The partner common to both pathways, Smad4, and inhibitory Smads (Smad6 and Smad7) play important roles. BMP bone morphogenetic protein, ALK1 activin receptor-like-kinase 1, ALK5 activin receptor-like kinase 5