Another Piece in the Fibrotic Puzzle: TSLP as a Novel Ligand for Fibrocyte Activation

Abstract

Thymic stromal lymphopoietin (TSLP) has emerged as an important cytokine in the pathogenesis of nonallergic diseases, especially in diseases that include fibrosis. It has been shown to be upregulated in both cutaneous and lung fibrotic conditions. Shin et al. report that TSLP may also play a role in the pathogenesis of keloids. The main mechanism of TSLP profibrotic effects is not as yet fully understood, although the data suggest that it involves collagen production through transforming growth factor-β, at least in the case of dermal fibroblasts. The authors also report that TSLP is able to activate fibrocytes, probably by inducing stromal cell-derived factor-1 (also termed CXCL12), one of its main ligands. These findings support the concept that TSLP plays a role in the development of fibrosis, and they should lead to mechanistic studies on TSLP profibrotic signaling.

Genistein inhibited endocytosis and fibrogenesis in transforming growth factor-β1-stimulated keloid via CTGF signaling pathways

“…Transforming growth factor-β (TGF-β) is a versatile protein orchestrating various cellular processes, including cell growth, differentiation, motility, and extracellular matrix production during normal wound healing. However, its dysregulation has been associated with excessive scar formation and brotic disorders (4)(5)(6). Elevated levels of TGF-β1 can trigger broproliferative disorders by promoting collagen synthesis, thereby exacerbating keloid formation.…”