Mechanically, PGC-1α deletion induces higher rates of tubular cell death, compensatory proliferation, expression of proinflammatory cytokines, NF-κB activation, and interstitial inflammatory cell infiltration.508 Conversely, in the cisplatin-induced AKI model, overexpression of PGC-1α or PGC-1α activator (ZLN005) treatment blocks cell apoptosis and mitochondrial dysfunction, finally alleviating kidney injury. This evidence concerns the gene PPARGC1A and acute kidney injury.