Transcriptomic profiling of mouse kidneys following ischemia-reperfusion injury
Acute kidney injury (AKI) is a major global health burden, and renal ischemia-reperfusion injury (RIRI) is its predominant cause. The molecular mechanisms driving post-ischemic renal injury and maladaptive repair remain incompletely understood. The primary goal of this study was to elucidate the specific regulatory role of TRIM29 during RIRI at the transcriptomic level. To achieve this, we performed RNA-sequencing on kidney tissues from TRIM29 conditional knockout (CKO) mice and TRIM29 Flox/Flox control mice subjected to RIRI operations. By mapping the differential gene expression landscape between these genotypes under ischemic stress, we aimed to uncover how TRIM29 deficiency alters pathogenic pathways. These transcriptomic data provide valuable insights into downstream signaling cascades, particularly the MAPK signaling pathway, ubiquitination processes, and inflammatory responses that dictate tubular epithelial cell survival. Ultimately, this dataset serves as a crucial resource for understanding TRIM29-mediated protective mechanisms and discovering promising therapeutic targets for AKI.