Identification of TACSTD2 as novel therapeutic targets for cisplatin-induced acute kidney injury by multi-omics data integration

In this study, after initially processed individual omics datasets, we integrated multi-omics data to construct a ferroptosis network in the kidney, resulting in the identification of the key driverTACSTD2. In vitro and in vivo results showed thatTACSTD2 was notably upregulated in cisplatin-treated kidneys and BUMPT cells. Overexpression ofTACSTD2 accelerated ferroptosis, while its gene disruption decelerated ferroptosis, likely mediated by its potential downstream targetsHMGB1, IRF6, andLCN2. Drug prediction and molecular docking were further used to propose that drugs targetingTACSTD2 may have therapeutic potential in CP-AKI, such as parthenolide, progesterone, premarin, estradiol and rosiglitazone. Our findings suggest a significant association between ferroptosis and the development of CP-AKI, withTACSTD2 playing a crucial role in modulating ferroptosis, which provides novel perspectives on the pathogenesis and treatment of CP-AKI.
Source: Human Genetics - Category: Genetics & Stem Cells Source Type: research