Inhibition of methylthioadenosine phosphorylase provides protection from experimental acute kidney injury

This dataset presents transcriptomic profiling of mouse kidney cortex in a model of ischemia-reperfusion injury (IRI) with and without methylthioadenosine phosphorylase (MTAP) inhibition (MTAPi). Male C57BL/6J mice were assigned to sham (n=6), IRI with vehicle (n=6), or IRI with MTAP inhibitor (MTAPi; n=5) groups. MTAPi (MT-DADMe-ImmA, AdooQ Bioscience, Cat# A13651) was administered intraperitoneally 4.5 hours before ischemia. Total RNA was extracted from kidney cortices, depleted of rRNA, and processed using a directional library prep kit. Libraries were sequenced on the Illumina NovaSeq 6000 platform (100 bp paired-end). Transcriptomic analysis revealed that MTAP inhibition reduced injury-associated gene expression, suppressed inflammatory and stress pathways, and preserved epithelial and metabolic gene programs. These data provide insight into the protective role of MTAP inhibition in acute kidney injury. Male C57BL/6J mice (10–12 weeks old) were assigned to three groups: sham surgery (n=6), ischemia-reperfusion injury (IRI) with vehicle (n=6), and IRI with MTAP inhibitor (MTAPi) treatment (n=5). IRI was induced by clamping both renal pedicles for 30 minutes, followed by 24 hours of reperfusion. MTAPi (MT-DADMe-ImmA, AdooQ Bioscience, Cat# A13651, 20 mg/kg) or vehicle (10% DMSO in PBS) was administered intraperitoneally 4.5 hours before ischemia. Kidney cortex tissue was collected for RNA extraction (QIAGEN RNeasy Mini Kit, Cat# 74104), rRNA depletion, and directional RNA library preparation. Libraries were sequenced using the Illumina NovaSeq 6000 with 100 bp paired-end reads.