Identifying new cellular mechanisms of mineralocorticoid receptor activation in the heart

Recent studies have expanded our understanding of the actions of the mineralocorticoid receptor (MR) to a diverse array of tissue types that differ substantially from the epithelial cells of the renal nephron. In these cell types the role of the MR has been largely, but not exclusively, defined in terms of pathogenic signalling pathways leading to tissue injury and remodelling. Macrophages and cardiomyocytes are two cell types in which the MR plays a central role in the cardiac tissue response to injury, renovascular hypertension and oxidative stress for example. Macrophages are critical for resolution of tissue injury and wound healing and their pleiotropic actions are central to the development of many forms of heart, renal and vascular disease. The MR in cardiomyocytes is not only essential for the chronotropic and ionotropic actions of mineralocorticoids in the short and longer term, but also for induction of hypertrophic and proinflammatory signalling programs. The present review discusses recent studies, presented at the Aldosterone and Hypertension Satellite of the 15th Asian-Pacific Congress of Hypertension, investigating new mechanisms for MR signalling in these cells and how their dysfunction contributes to the onset and progression of cardiovascular disease and heart failure.

Automated summary

Recent studies have shown that the mineralocorticoid receptor (MR) plays a crucial role in various tissue types beyond renal epithelial cells, where its actions are mainly defined in the context of pathogenic signaling pathways leading to tissue injury and remodeling. Macrophages and cardiomyocytes are two cell types where the MR is central in the tissue response to factors like injury, renovascular hypertension, and oxidative stress. The dysfunction of MR in these cells contributes to the onset and progression of cardiovascular disease and heart failure.