Single-Cell Multi-Omics in Chronic Kidney Disease: Mechanistic Insights into Renal Fibrosis, Inflammatory Remodeling, and Precision Therapeutics
Abstract
Chronic kidney disease (CKD) represents a progressive and multifactorial
disorder characterized by persistent renal injury, inflammatory remodeling,
fibrosis, and irreversible decline in kidney function. Despite substantial
advances in nephrology, the molecular complexity and cellular
heterogeneity underlying CKD progression remain incompletely
understood, thereby limiting the development of effective targeted
therapies. Recent innovations in single-cell multi-omics technologies have
transformed the understanding of renal pathophysiology by enabling high-
resolution characterization of transcriptional, epigenomic, proteomic,
metabolomic, and spatial alterations within individual kidney cell
populations. These approaches have uncovered dynamic interactions
among tubular epithelial cells, fibroblasts, endothelial cells, immune
populations, and stromal compartments that collectively drive fibrosis and
chronic inflammation. Single-cell analyses further reveal profound cellular
plasticity, maladaptive repair mechanisms, metabolic reprogramming, and
immune dysregulation contributing to progressive renal injury.
Importantly, integrative multi-omics approaches have facilitated the
identification of novel biomarkers, pathogenic signaling pathways, and
therapeutic vulnerabilities suitable for precision nephrology strategies.
Emerging computational platforms, artificial intelligence-assisted analyses,
and spatial transcriptomic technologies are additionally enhancing
understanding of intrarenal cellular communication and disease
heterogeneity. This review discusses the current landscape of single-cell
multi-omics in CKD, emphasizing mechanistic insights into renal fibrosis,
inflammatory remodeling, cellular heterogeneity, and emerging
translational opportunities for personalized therapeutic intervention.
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