SMADS-Mediate Molecular Mechanisms in Sjögren’s Syndrome

International Journal of Molecular Sciences

Domenico Ribatti¹  Sabrina Lisi¹  Margherita Sisto¹ 

[1] Department of Basic Medical Sciences, Neurosciences and Sensory Organs (SMBNOS), Section of Human Anatomy and Histology, University of Bari “Aldo Moro”, I-70124 Bari, Italy;

关键词: SMAD;    Sjögren’s syndrome;    epithelial-mesenchymal transition;    fibrosis;    TGF-β;    inflammation;   

DOI  :  10.3390/ijms22063203

来源: DOAJ

【 摘 要 】

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 Sjögren’s syndrome (pSS) has been focused on inflammation, but, recently, the involvement of TGF-β/SMADs signalling has been demonstrated in pSS salivary glands (SGs) as mediator of the epithelial-mesenchymal transition (EMT) activation. Although EMT seems to cause pSS SG fibrosis, TGF-β family members have ambiguous effects on the function of pSS SGs. 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.

【 授权许可】

Unknown