Clinical Immunology and Immunopathology
Regular ArticleIncreased Synovial Expression of Transforming Growth Factor (TGF)-β Receptor Endoglin and TGF-β1 in Rheumatoid Arthritis: Possible Interactions in the Pathogenesis of the Disease
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2019, PhytomedicineCitation Excerpt :On the other hand, TGF-β1 is one of the most powerful and widely distributed profibrogenic mediators in the body. A previous research has indicated enhanced expression of TGF-β1 protein in RA synovial, and it may be related with active pathological changes in RA synovia including synoviocyte hyperplasia, inflammatory cell infiltration and granuloma formation (Dai et al., 2000; Szekanecz et al., 1995). In addition, data from other reports have shown that systemic inhibition of TGF-β1 signalling can significantly reduce the severity of synovitis in RA animal models, likely by suppressing TGF-β1-mediated synoviocytes proliferation and endothelial angiogenesis (Sakuma et al., 2007; Wahl et al., 1993).
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2013, Biochimica et Biophysica Acta - Molecular Basis of DiseaseCitation Excerpt :Some studies would support the idea of that endoglin and ALK-1 participate in a common signaling pathway and endoglin would potentiate TGF-β/ALK-1 signaling through a direct association of ALK-1 with the cytoplasmic and extracellular domain of endoglin [121]. Endoglin is highly expressed in vascular endothelial cells at sites of active angiogenesis, during embryogenesis [140,141], in healing wounds and inflammation processes [101,142], upon vascular injury [143], and in cancer [136,144–146]. It has also been described to be overexpressed after ischemia and reperfusion in kidney, heart or hindlimbs [102,147,148].