SLC31A1 and hydrops fetalis: Additionally, an <i>in vitro</i> model of hypoxia was induced in macrophages RAW264.7, which were then treated with small interfering RNA targeting SLC31A1, ATTM and nigericin, and subsequently co-cultured with cardiomyocytes to validate the SLC31A1 mechanism <i>in vitro</i>.<h4>Results</h4>SLC31A1 was up-regulated in macrophages of mice with post-AMI HF , while its knockdown prevented cardiomyocyte apoptosis and post-AMI HF.