Menopause-induced estrogen depletion contributes to the development of heart failure with preserved ejection fraction through dysregulation of the renin-angiotensin system and chronic inflammation.
What are the pathophysiological alterations observed in HFpEF induced by menopause and what are the potential therapeutic targets?
This review highlights the pathophysiological mechanisms linking estrogen depletion during menopause to the development of HFpEF and identifies potential therapeutic targets.
Aging is an important risk factor for the development of heart failure (HF) and half of patients with HF have preserved ejection fraction (HFpEF) which is more common in elderly women. In general, sex differences that lead to discrepancies in risk factors and to the development of cardiovascular disease (CVD) have been attributed to the reduced level of circulating estrogen during menopause. Estrogen receptors adaptively modulate fibrotic, apoptotic, inflammatory processes and calcium homeostasis, factors that are directly involved in the HFpEF. Therefore, during menopause, estrogen depletion reduces the cardioprotection. Preclinical menopause models demonstrated that several signaling pathways and organ systems are closely involved in the development of HFpEF, including dysregulation of the renin-angiotensin system (RAS), chronic inflammatory process and alteration in the sympathetic nervous system. Thus, this review explores thealterations observed in the condition of HFpEF induced by menopause and the therapeutic targets with potential to interfere with the disease progress.
Silva et al. (Thu,) conducted a review in Heart failure with preserved ejection fraction (HFpEF) in menopause. Menopause-induced estrogen depletion contributes to the development of heart failure with preserved ejection fraction through dysregulation of the renin-angiotensin system and chronic inflammation.