Since its discovery and introduction in early 1980s, the glucocorticoid antagonist mifepristone (RU 486) has been studied in several clinical conditions. However, it has also caused great controversy in clinical practice. This is because the xenobiotic acts as a progesterone antagonist by competing with endogenous progesterone for receptor binding. Nevertheless, the role of apoptosis induced by mifepristone in cardiomyocytes is not fully understood so far. This article reports the new argument on the putative impact of apoptosis induced by mifepristone in cardiomyocytes. Certainly, these consequences can cause important implications for human health.
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