For example, in a cisplatin-induced acute kidney injury model, SQOR deficiency exacerbated mitochondrial dysfunction and lipid peroxidation in renal tubular cells, significantly increasing ferroptotic cell death and tissue damage; conversely, normal SQOR activity eliminated excess sulfide and preserved CoQ10H2’s antioxidant function, thereby mitigating cisplatin-induced oxidative damage and protecting the kidney (Cai et al., 2024). Here, SQOR is linked to acute kidney injury.