Myeloid FtH deficiency accelerates kidney disease by inducing Snca and ferroptosis [Fe treatment WT-KO]

Following kidney injury, we observed increased iron depsoition in kidneys of myeloid specific FtH deficient (FtHΔ/Δ) mice when compared to wild-type (FtHfl/fl) kidneys. To explore mechanisms coordinating increased iron accumulation in FtHΔ/Δ kidneys, we employed a parenterally induced iron overload model by injecting 10–12-week-old male FtHfl/fl (wild-type) and FtHΔ/Δ (myeloid-specific FtH-deficient) mice with 0.4 mg/g body weight iron dextran via five intraperitoneal injections on consecutive days. Three days after the final injection, kidneys were harvested and sent for bulk RNA sequencing to assess transcriptional changes underlying tissue iron deposition due to FtH deletion in myeloid cells. Total RNA was isolated from kidney of wild-type (FtHfl/fl) n=4 and myeloid specific FtH deficient (FtHΔ/Δ) n=4 mice treated with iron using Trizol. We then perfomed gene expression profilling analysis using RNA -Seq