Transcriptomic profiling of the mouse retina reveals the protective mechanism of Liproxstatin-1 against ischemia-reperfusion injury
Retinal ischemia-reperfusion (I/R) injury is a common pathological process in various ocular diseases, leading to neuronal death and vision loss. Ferroptosis, an iron-dependent form of regulated cell death, has been implicated in I/R injury. This study aims to investigate the therapeutic potential and underlying molecular mechanisms of Liproxstatin-1 (Lip-1), a potent ferroptosis inhibitor, in a mouse model of retinal I/R injury.We performed bulk RNA sequencing on retinal tissues from three experimental groups: (1) Normal control mice, (2) Mice subjected to retinal I/R injury, and (3) I/R mice treated with Liproxstatin-1. Comparative transcriptomic analysis was conducted to identify differentially expressed genes (DEGs) and altered signaling pathways between these groups.The dataset provides comprehensive gene expression profiles that elucidate how Liproxstatin-1 modulates transcriptional networks involved in ferroptosis, inflammation, oxidative stress, and apoptosis following retinal I/R. Key findings are expected to highlight the crucial pathways targeted by Lip-1, such as the GPX4-GSH axis and associated lipid peroxidation pathways, thereby supporting its role as a neuroprotective agent. This resource will facilitate further research into ferroptosis-targeted therapies for retinal neuroprotection.