International Journal of Surgery

Authors
Weixin Zhang, Francisco Lopez, Mei Wan, Junying Zheng, Russell Wesson, Zhaoli Sun, Xu Cao


Lab

Journal
International Journal of Surgery

Abstract
Emerging evidence identifies immune dysregulation, fibroblast-like synoviocyte (FLS) activation, and pathological neurovascular remodeling as key drivers of RA pathogenesis[9–11]. Transforming Growth Factor Beta (TGF-β) signaling plays a complex, context-dependent role, functioning as both an immunoregulatory and pathogenic factor. TGF-β1 is upregulated in the synovium of RA patients – including in synovial lining cells, macrophages, and endothelial cells – and is elevated in synovial fluid compared to osteoarthritis and healthy controls[12–14]. In RA, TGF-β promotes Th17 cell differentiation in the presence of IL-6, contributes to synovial fibrosis and hyperplasia, and enhances pathological angiogenesis[15–17]. In conjunction with inflammatory cytokines such as TNF-α, IL-1β, and IL-6, TGF-β upregulates receptor activator of NF-κB ligand (RANKL) in FLSs, promoting osteoclastogenesis and bone erosion[18,19]. The imbalance between pro-inflammatory Th17 cells and regulatory T cells (Tregs), alongside elevated TNF-α and IL-17A, further perpetuates chronic inflammation and joint destruction[8,20]. Additionally, aberrant angiogenesis and sensory nerve innervation within the synovial microenvironment exacerbate joint pain. Targeting the TGF-β pathway and its downstream mediators (e.g., SMADs) offers therapeutic potential but requires selective modulation to preserve essential immunoregulatory functions, such as Treg maintenance.

Keywords/Topics
pathological neurovascular remodeling; joint pain; surgery; immune dysregulation; fibroblast-like synoviocyte fls activation; key drivers; transforming growth factor beta; tgf-β; tgf-β1; ra patients

Source :

https://journals.lww.com/international-journal-of-surgery/fulltext/9900/mobilizing_stem_cells_and_inhibition_of.4902.aspx

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