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Integrating Multi-Omics Data Using Machine Learning to Explore New Therapeutic Targets for Acute Kidney Injury

Qiming Gong1,2, Yakun Wang3,4, Fahui Liu5

  • 1Department of Nephrology, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, China.

Journal of Cellular and Molecular Medicine
|August 27, 2025
PubMed

Insights

Renal ischemia-reperfusion (I/R) injury, a complication of kidney transplants, lacks targeted treatments. This study identifies ADAMTS1 as a key factor in I/R-induced acute kidney injury (I/R-AKI) and shows troglitazone can mitigate damage.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Bioinformatics

Background:

  • Renal ischemia-reperfusion (I/R) injury is a significant complication in renal transplantation, leading to acute kidney injury (AKI).
  • Current therapeutic strategies for I/R-AKI are limited, necessitating the identification of novel molecular targets and diagnostic tools.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying I/R-induced AKI (I/R-AKI) at the single-cell level.
  • To identify potential therapeutic targets and develop diagnostic models for I/R-AKI.
  • To evaluate the efficacy of pharmacological agents in mitigating I/R-AKI.

Main Methods:

  • Bioinformatic analysis of single-cell data to identify critical genes in I/R-AKI.
  • Development and validation of a diagnostic model for I/R-AKI.
  • Experimental validation using immunofluorescence, western blotting, immunohistochemistry, and transmission electron microscopy in I/R mouse models and human AKI samples.
  • Assessment of troglitazone's effect on ADAMTS1 expression and I/R-AKI pathology.

Main Results:

  • A robust diagnostic model for I/R-AKI was developed and validated.
  • ADAMTS1 was identified as a promoter of renal I/R-AKI, significantly upregulated in renal tubular epithelial cells.
  • Mitochondrial pathway-mediated apoptosis was confirmed as a critical factor in I/R injury progression.
  • Inhibition of ADAMTS1 by troglitazone significantly reduced functional and histological damage in I/R-AKI mouse models.

Conclusions:

  • ADAMTS1 plays a crucial role in promoting renal I/R-AKI.
  • The developed diagnostic model is valuable for I/R-AKI diagnosis.
  • Troglitazone demonstrates therapeutic potential for I/R-AKI by inhibiting ADAMTS1 expression, offering insights for future treatment strategies.
Keywords:
ADAMTS1apoptosisrenal ischemia–reperfusion injurysingle‐celltroglitazone

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