Advances in focal segmental glomerulosclerosis research: genetic causes to non-coding RNAs

Focal Segmental Glomerulosclerosis (FSGS) is a clinicopathological illness characterized by podocyte damage, impairing glomerular filtration, and substantial proteinuria, which often results in end-stage renal disease (ESRD). Divided into primary, secondary, genetic, and idiopathic categories, its diverse origin highlights the intricacy of its diagnosis and treatment. The existing dependence on immunosuppressive medicines highlights their side effects and inconsistent efficacy, underscoring the pressing necessity for innovative, focused treatments. Recent advancements in genomics and molecular biology have shown the significant involvement of genetic alterations, especially in podocyte-associated proteins, in the pathogenesis of FSGS. Identifying possible novel biomarkers for diagnosing FSGS and monitoring disease activity has revitalized interest in this condition. Recent data underscores the significance of non-coding RNAs, including microRNAs (miRNAs), circular RNAs (circRNAs), and long non-coding RNAs (lncRNAs), in the modulation of gene expression and podocyte functionality. Particular dysregulated miRNAs and circRNAs have demonstrated potential as biomarkers for early diagnosis and disease monitoring. Furthermore, understanding lncRNA-mediated pathways provides novel therapeutic targets. This review consolidates current progress in elucidating the genetic and molecular processes of FSGS, emphasizing biomarker identification and treatment innovation.