Аңдатпа
Renal fibrosis is a major morphological feature of chronic kidney disease and is considered an important pathogenetic process that leads to a decline in renal function in the progressive course of the disease. It is characterized by excessive accumulation of extracellular matrix, tubular atrophy, interstitial inflammation, capillary thinning, and nephron structural disruption. The development of fibrosis involves transforming growth factor-β (TGF-β), Wnt/β-catenin, inflammatory mediators, and intercellular communication between macrophages and activated fibroblasts. TGF-β, as one of the main driving factors of renal fibrosis, enhancing the activation of myofibroblasts and the accumulation of extracellular matrix proteins such as collagen and fibronectin through Smad-dependent and Smad-independent pathways. Collagen Triple Helix Repeat Containing 1 (CTHRC1), a secreted glycoprotein, was initially described in vascular remodeling and tissue repair processes after injury, and later studies began to consider it as a regulatory molecule in fibrotic diseases. The high expression of CTHRC1 protein in renal tissue in tubular cells and undetectable levels in glomerular cells provide a basis for investigating its association with tubulointerstitial injury in the kidney. CTHRC1 may be involved in fibroblast migration, tissue remodeling, extracellular matrix metabolism, and interaction with the TGF-β/Wnt signaling systems during kidney fibrogenesis. This review discusses the potential role of CTHRC1 in renal fibrosis, its relationship with the TGF-β and Wnt/β-catenin pathways, and its potential as a diagnostic biomarker and therapeutic target in chronic kidney diseases.