Strikingly, NLRP3/HMGB1 activation in vivo partly abolished SLC31A1 knockdown-induced alleviation of macrophage cuproptosis and cardiomyocyte apoptosis.<h4>Discussion</h4>SLC31A1 plays a disease-promoting role in HF after AMI by activating NLRP3/HMGB1-dependent macrophage cuproptosis, which is expected to be a potential biomarker for HF. This evidence concerns the gene NLRP3 and hydrops fetalis.