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Sex Differences in Remodeling of the Failing Heart

Heart failure (HF) is a leading cause of hospitalization and death and can be characterized by either reduced or preserved ejection fraction. Cardiomyopathies like Takotsubo and HF manifest differently between men and women. More men have maladaptive remodeling underlain by higher induction of pro‐fibrotic pathways, while women repress inflammatory pathways. Sex and menopause‐related differences in the incidence and the prognosis of cardiovascular disease have pointed to the sex hormone 17β‐estradiol (E2) and its receptors (ER α and β). Employing the transverse aortic constriction model in mice to study E2‐ and sex‐specific regulation of pressure overload‐induced left ventricular hypertrophy and HF, the E2/ER axis is considered cardioprotective in females. In contrast, E2 exerts deleterious effects in male hearts and cardiac cells. Detailed characterization of the regulation of cardiac (patho)physiology by sex and E2 and elucidation of the underlying mechanisms may lead to the identification of novel therapeutic targets, which may have a wide implication in the development of new and personalized therapies.