In sepsis-associated cardiotoxicity, remifentanil reduces oxidative stress, inflammation, and apoptosis to maintain mitochondrial biogenesis by inhibiting NFkB and cas-3 immunoexpressions and enhancing SIRT1 upregulation

REMI exhibits significant cardioprotective effects in LPS-induced SIC by attenuating inflammation, oxidative stress, and apoptosis while preserving mitochondrial homeostasis.