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May 22, 2026Current Research in ToxicologyOpen Access

Loss of KLF15 expression characterizes proximal tubule injury in cisplatin-induced acute kidney injury: A multi-omics study

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Authors

LCLei ChenSXShiying XieHYHeqing Yang

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Overview

Randomized trial reveals loss of KLF15 links to inflammation in acute kidney injury, implying potential therapeutic targets.

Key Points

  • This study aims to identify transcription factors involved in cisplatin-induced acute kidney injury and explore possible therapeutic agents.
  • Integrative multi-omics analysis using bulk RNA-seq, proteomic, and single-cell RNA-seq datasets.
  • Validation of KLF15 expression in a cisplatin-induced acute kidney injury mouse model.
  • Molecular docking to screen FDA-approved drugs targeting KLF15.
  • KLF15 was downregulated in cisplatin-induced acute kidney injury (AKI) with Klf15 mRNA and protein levels markedly reduced.
  • Loss of Klf15 in proximal tubule cells correlated with increased inflammation and apoptosis with suppressed metabolic pathways.
  • Molecular docking identified 6 drugs, including Simeprevir, as potential compounds targeting KLF15.

Cite This Study

Chen et al. (2026) studied this question.

synapsesocial.com/papers/6a0ff2cdd674f7c03778b532https://doi.org/10.1016/j.crtox.2026.100300
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