Transforming growth factor-β1 (TGF-β1)/Smad signaling pathway. TGF-β1 can activate Smad 2/3 by binding to the membrane-bound TGF-β1 receptor (TβR). Thereafter, Smad 2/3 bound to Smad 4 enters the nucleus and regulates target gene transcription. Smad 7 can bind to the TβR and inhibit the activation of Smad signaling [1].
Reference
Hu, D. et al. Human ucMSCs seeded in a decellularized kidney scaffold attenuate renal fibrosis by reducing epithelial–mesenchymal transition via the TGF-β/Smad signaling pathway. Pediatr. Res. https://doi.org/10.1038/s41390-019-0736-6 (2020).
Author information
Authors and Affiliations
Corresponding author
Additional information
Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Rights and permissions
About this article
Cite this article
Hu, D., Zhang, D., Liu, B. et al. Insights Image for “Human ucMSCs seeded in a decellularized kidney scaffold attenuate renal fibrosis by reducing epithelial-mesenchymal transition via the TGF-β/Smad signaling pathway”. Pediatr Res 88, 336 (2020). https://doi.org/10.1038/s41390-020-0847-0
Received:
Accepted:
Published:
Issue Date:
DOI: https://doi.org/10.1038/s41390-020-0847-0