RNA-seq of primary cardiomyocytes under ischemia-reperfusion injury reveals altered expression in DNA damage repair genes including Xrcc6

To investigate the molecular response of cardiomyocytes to ischemia-reperfusion (I/R) injury, we established an in vitro I/R model using primary neonatal mouse cardiomyocytes. Oxidative stress was simulated by treating the cells with 100 μM hydrogen peroxide (H₂O₂) for 24 hours, followed by a 24-hour recovery period in complete medium to mimic the ischemia and reperfusion phases, respectively. Bulk RNA sequencing was performed on both control (n = 3) and I/R-treated (n = 4) cardiomyocytes. Transcriptomic profiling identified differentially expressed genes and enriched pathways associated with oxidative stress response, DNA damage repair, and regulation of cell death. This dataset provides valuable insights into the molecular mechanisms underlying myocardial I/R injury and may help identify potential therapeutic targets. Primary cardiomyocytes were isolated from 1–3-day-old C57BL/6 neonatal mice and cultured under standard conditions. The ischemia-reperfusion (I/R) injury model was induced in vitro using 100 μM H₂O₂ in serum-free medium for 24 hours to simulate ischemia, followed by replacement with normal culture medium for another 24 hours to mimic reperfusion. RNA was extracted from untreated control (n=3) and I/R-injured(n=4) cells, and RNA-seq libraries were constructed using the VAHTS Universal V5 RNA-seq Library Prep Kit. Sequencing was performed on the Illumina NovaSeq 6000 platform. Differential expression and pathway analyses were conducted to identify genes associated with oxidative stress, DNA damage, and potential drug targets.