ArticleCurrent research in toxicology2026
Loss of KLF15 expression characterizes proximal tubule injury in cisplatin-induced acute kidney injury: A multi-omics study.
Article in Current research in toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Impaired fatty acid metabolism in AKI: experimental evidence - a narrative review.BMC nephrology · 2026Review
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6 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Nephrotoxicity is a common side effect of cisplatin (CSP), a widely-used anti-tumor chemotherapy drug. Acute kidney injury (AKI) induced by it is characterized by inflammation, apoptosis, and metabolic reprogramming in proximal tubule (PT) cells. However, the key pathways and upstream transcriptional regulators orchestrating these pathological changes remain poorly understood. This study aimed to identify crucial transcription factors (TFs) involved in CSP-induced AKI and to explore potential therapeutic agents targeting them. An integrative multi-omics analysis of public bulk RNA-seq, proteomic, and single-cell RNA-seq datasets was performed to identify dysregulated pathways and key TFs. The expression of Krüppel-like factor 15 (KLF15), the lead candidate TF, was validated in a CSP-induced AKI mouse model (20 mg/kg intraperitoneal injection for 72 h) using RT-qPCR and Western blot. Molecular docking utilizing AutodockVina was employed to virtually screen an FDA-approved drug library for potential compounds targeting KLF15.Transcriptomics and proteomics analyses consistently identified KLF15 as a top-ranked, downregulated TF in CSP induced AKI. Single-cell analysis revealed that PT cells were the most affected, and the loss of
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