Necrosis biomarkers are also closely related to inflammation and oxidative stress biomarkers, and myocardial cell necrosis may also stimulate the formation of the oxidative stress marker C-reactive protein.72–76 RIPK1, caspase 8 and FADD interact to form the RIPK1-FADD-caspase 8 complex, which leads to necrotic cell death, cardiac pathological remodeling and HF.77,78 In this study, we demonstrated that 2-APQC can regulate the AMPK-Parkin axis to inhibit the formation of the RIPK-FADD-caspase 8 complex and reduce the necrosis of cardiomyocytes. This evidence concerns the gene FADD and hydrops fetalis.