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. 2022 Sep 28;28(36):5250–5264. doi: 10.3748/wjg.v28.i36.5250

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©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.

This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.

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Transforming growth factor-beta 1 signaling pathway. Smad and non-Smad pathways mainly regulate transforming growth factor-beta 1 (TGF-β1) signal transduction. Integrin signaling triggers the activation and release of TGF-β1 from LCC (large latent complex). Activated TGF-β1 binds TGF-β type II receptor, leading to phosphorylation of TGF-β type I receptor and associated Smad proteins, mainly Smad-2 and Smad-3. Phosphorylated Smad-2 and 3, complex with the co-Smad, Smad-7, form a ternary complex. This ternary complex then translocates into the nucleus, binds to Smad binding elements and regulates the transcription of TGF-β-related genes. TGF: Transforming growth factor; LAP: Latency associated protein; LTAB: Latent transforming growth factor-beta binding protein; SBE: Smad binding elements; ECM: Extracellular matrix; mTOR: Mammalian target of Rapamycin; PI3K: Phosphoinositide 3-kinase; AKT: AKT serine/threonine kinase 1; MKK: Mitogen-activated protein kinase kinase; JNK: C-Jun N-terminal kinase.