The angiotensin II receptor antagonist telmisartan promotes renal recovery after ischemia-reperfusion injury by reprogramming fatty acid metabolism

RAAS inhibitors are routinely withheld during acute kidney injury (AKI) because of concerns about impaired renal perfusion. Contrary to this dogma, we show that telmisartan enhances renal recovery following ischemia-reperfusion injury. Transcriptomic analyses reveal that telmisartan restores fatty acid oxidation and mitochondrial-peroxisomal lipid metabolism, key pathways suppressed in AKI. These findings suggest that selected RAAS inhibitors may actively promote post-AKI metabolic recovery rather than merely pose hemodynamic risk.