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REVIEW article
Front. Physiol.
Sec. Craniofacial Biology and Dental Research
Volume 16 - 2025 | doi: 10.3389/fphys.2025.1586769
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Amelogenesis is a highly regulated process involving multiple signaling pathways, among which the transforming growth factor-β1 (TGF-β1) signaling pathway plays a pivotal role in enamel formation. This review firstly elucidates the critical functions of TGF-β1 in regulating ameloblast behavior and enamel development, encompassing ameloblast proliferation, differentiation, apoptosis, enamel matrix protein synthesis, and mineralization. Secondly, based on emerging evidence, we further discuss potential interactions between TGF-β signaling and circadian regulation in enamel formation, although this relationship requires further experimental validation. Finally, future research directions are proposed to further investigate the relationship between TGF-β1 and the circadian clock in the context of amelogenesis.
Keywords: Amelogenesis, TGF-β1, Circadian clock, ameloblast, Enamel formation, Enamel development
Received: 03 Mar 2025; Accepted: 31 Mar 2025.
Copyright: © 2025 Ma, Ma, Lin and Ji. 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) or licensor 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.
* Correspondence:
Mei Ji, Department of Stomatology Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan,Shandong, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.
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