MCL1 and acute kidney injury: For validation, AAV-mediated tubular-specific USP13 overexpression will be used in cisplatin-induced AKI mice to detect mitochondrial function (such as reactive oxygen species levels and mitochondrial membrane potential) and renal injury markers (including serum creatinine and tubular apoptosis rate); in vitro, tubular epithelial cells treated with USP13 agonists will be used to verify the effects of USP13 activation on MCL-1 stability and mitochondrial injury [100,121].