ArticleRenal failure2026
Integrative transcriptomic and single-cell analyses identify CD74 as a candidate regulator of ferroptosis in renal tubular cells during nephrolithiasis.
Article in Renal failure, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Nephrolithiasis incidence has risen with frequent recurrence, and injury to renal tubular epithelial cells is central to its pathology. Ferroptosis, an iron-dependent form of regulated cell death, has been implicated in kidney diseases, but its role in nephrolithiasis remains unclear. In this study, we investigated whether CD74 is associated with ferroptosis-related tubular injury during nephrolithiasis and explored the potential involvement of NF-κB signaling. A glyoxylate-induced mouse model showed prominent calcium oxalate deposition, impaired renal function, altered expression of ACSL4 and GPX4, and increased oxidative stress. Integrating bulk transcriptomics, protein-protein interaction networks, bioinformatics, and a public single-cell RNA-sequencing dataset, we identified CD74 as a candidate ferroptosis-associated gene showing increased expression during nephrolithiasis progression.
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