Ex vivo studies revealed that AT<sub>2</sub>R agonist promoted CD4<sup>+</sup> cell expansion into Tregs, which was blocked by the AT<sub>2</sub>R antagonist PD123319, PP2A inhibitor okadaic acid, or NO synthase inhibitor L-NAME, suggesting the direct involvement of AT<sub>2</sub>R-PP2A-NOS pathways.<h4>Discussion</h4>Overall, AT<sub>2</sub>R activation reduces M1 and promotes Tregs accumulation in IR-AKI, thus shifting the kidney microenvironment towards anti-inflammation and presents a potential mechanism to limit kidney injury and promote repair. Here, PTPA is linked to acute kidney injury.