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Inhibition of methylthioadenosine phosphorylase protects from experimental acute kidney injury

Afaf Saliba1,2, Yidong Chen3,4, Jonathan W Nelson5

  • 1Center for Precision Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States.

American Journal of Physiology. Renal Physiology
|July 2, 2025
PubMed

Insights

Prophylactic inhibition of methylthioadenosine phosphorylase (MTAP) protects against experimental acute kidney injury (AKI) in mice. MTAP inhibition suppressed stress and maladaptive repair pathways, suggesting MTAP as a therapeutic target for AKI.

Area of Science:

  • Nephrology
  • Biochemistry
  • Molecular Biology

Background:

  • Methylthioadenosine phosphorylase (MTAP) is crucial in purine metabolism and influences cellular injury responses.
  • Acute kidney injury (AKI) involves complex cellular stress and repair mechanisms.

Purpose of the Study:

  • To investigate the therapeutic potential of prophylactic MTAP inhibition in mouse models of AKI.
  • To elucidate the molecular mechanisms underlying MTAP's role in kidney injury and repair.

Main Methods:

  • Utilized mouse models of ischemia-reperfusion and cisplatin-induced AKI.
  • Assessed MTAP inhibition via methylthioadenosine accumulation.
  • Performed transcriptomic analysis and analyzed human single-cell RNA sequencing data from AKI biopsies.

Main Results:

  • MTAP inhibition significantly reduced renal injury and tubular damage in mice.
  • Transcriptomic analysis revealed suppression of inflammatory and stress pathways, with preserved oxidative phosphorylation and epithelial integrity genes.
  • Human AKI data showed high MTAP expression in adaptive proximal tubule cells with mixed reparative and maladaptive features.

Conclusions:

  • Prophylactic MTAP inhibition demonstrates protective effects against experimental AKI.
  • MTAP inhibition modulates gene expression related to epithelial stress and maladaptive repair.
  • MTAP is identified as a promising therapeutic target for AKI treatment, particularly in specific kidney tubule subpopulations.
Keywords:
acute kidney injuryexperimental acute kidney injurymethylthioadenosine phosphorylaseprophylactic treatmentproximal tubules

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