Testosterone Protects Female Embryonic Heart H9c2 Cells Against Severe Metabolic Stress by Activating Estrogen Receptors and Up-Regulating IES SUR2B

The study found that testosterone protected female embryonic heart H9c2 cells from severe metabolic stress by activating estrogen receptors and up-regulating the mitochondrial sulfonylurea receptor 2B (IES SUR2B). This protective effect was likely due to testosterone's conversion into metabolites like estradiol, as it was not mediated through androgen receptors. The cytoprotection was dependent on new protein synthesis and was abolished by inhibitors like tamoxifene, finasteride, and anastrozole. The research suggested a novel mechanism of cardioprotection through the up-regulation of IES SUR2B, indicating potential therapeutic use of testosterone in females for conditions such as ischemic heart disease and heart failure. The study involved experiments with sample sizes ranging from 5 to 9.