Review
Version 1
Preserved in Portico This version is not peer-reviewed
SMADS-mediate Molecular Mechanisms in Sjӧgren's Syndrome
Version 1
: Received: 16 March 2021 / Approved: 17 March 2021 / Online: 17 March 2021 (14:43:37 CET)
A peer-reviewed article of this Preprint also exists.
Sisto, M.; Ribatti, D.; Lisi, S. SMADS-Mediate Molecular Mechanisms in Sjögren’s Syndrome. Int. J. Mol. Sci. 2021, 22, 3203. Sisto, M.; Ribatti, D.; Lisi, S. SMADS-Mediate Molecular Mechanisms in Sjögren’s Syndrome. Int. J. Mol. Sci. 2021, 22, 3203.
Abstract
There is considerable interest in delineating the molecular mechanisms of action of transforming growth factor-β (TGF-β), considered as central player in a plethora of human conditions, including cancer, fibrosis and autoimmune disease. TGF-β elicits its biological effects through membrane bound serine/threonine kinase receptors which transmit their signals via downstream signalling molecules, SMADs, which regulate the transcription of target genes in collaboration with various co-activators and co-repressors. Until now, therapeutic strategy for primary Sjӧgren’s syndrome (pSS) has been focused on inflammation, but, recently, the involvement of TGF-β/SMADs signalling has been demonstrated in pSS, although TGFβ family members seems to have ambiguous effects on the function of pSS salivary glands. Based on these premises, this review highlights recent advances in unravelling the molecular basis for the multi-faceted functions of TGF-β in pSS that are dictated by orchestrations of SMADs, and describe TGF-β/SMADs value as both disease markers and/or therapeutic target for pSS.
Keywords
SMAD; Sjӧgren’s syndrome; epithelial-mesenchymal transition; fibrosis; TGF-β; inflammation
Subject
Medicine and Pharmacology, Immunology and Allergy
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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