Irg1-itaconate axis protects against acute kidney injury via activation of Nrf2.

. Itaconate treatment promoted the survival of WT mice from lethal ischemia and protected against renal IRI and systemic inflammation. Mechanistically, dimethyl itaconate protected renal cells from oxidative stress and prevented macrophage activation by enhancing the translocation of Nrf2 into the nuclei. Our study highlighted the importance of the Irg1-itaconate axis in the protecting against ischemia-reperfusion injury and acute kidney injury, providing potential therapeutic targets to control AKI.