Fluorescent advanced glycation end products in the detection of factual stages of cartilage degeneration.

Chronic kidney disease (CKD) is a prevalent and progressive condition that leads to renal structural abnormalities and a gradual decline in kidney function. CKD has various etiologies, including diabetes, hypertension, and glomerulonephritis, and is associated with significant morbidity, mortality, and economic burden. Current treatments focus on slowing disease progression and managing complications; however, CKD often progresses to end-stage renal disease, necessitating renal replacement therapy. Therefore, innovative therapeutic approaches are urgently required. Recent studies have highlighted the role of ferroptosis, an iron-dependent form of cell death characterized by lipid peroxidation and oxidative stress, in CKD pathogenesis. Ferroptosis contributes to structural damage and functional impairment in renal cells. Furthermore, epigenetic modifications, including DNA methylation and histone changes, regulate gene expression without altering the DNA sequence and have been implicated in CKD progression. These epigenetic alterations may influence inflammation, fibrosis, and ferroptosis, thereby exacerbating renal dysfunction. This review explores the intersection of ferroptosis and epigenetic regulation in CKD, offering novel insights into the mechanisms driving disease progression and potential therapeutic targets. Through a comprehensive bibliometric analysis, this study provides a deeper understanding of CKD pathogenesis and proposes potential future treatment strategies.