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Kidney fibrosis is a progressive and maladaptive tissue repair process seen in chronic kidney disease, marked by excessive deposition of extracellular matrix such as collagens and fibronectin, tubular atrophy, infiltration of immune cells, transformation of perivascular cells into myofibroblasts, and vascular rarefaction, ultimately leading to irreversible renal failure. This process is orchestrated by multiple signaling molecules (notably TGF-β), profibrotic genes (e.g., Spp1), immune mediators (e.g., TNF), and epigenetic changes (e.g., DNA methylation, histone acetylation), and can be monitored using biomarkers or targeted through current and experimental antifibrotic therapeutics. Because it is a process—not a single molecule—the proper identification of molecular targets within the fibrosis pathway is essential for successful intervention and drug development.
Inhibition of TGF-β signaling; Blockade of profibrotic cytokines; Epigenetic modulation (HDAC/BET inhibition); Oxidative stress reduction; Anti-inflammatory effects; Inhibition of fibroblast activation and differentiation to myofibroblasts.
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