Cardiac Hypertrophy and Fibrosis in the Metabolic Syndrome: A Role for Aldosterone and the Mineralocorticoid Receptor

Figure 1

Proposed schematic representation of the interplay between adipose tissue, adrenal aldosterone production, and cardiac remodeling in the metabolic syndrome. Aldosterone production is increased in response to molecular factors including angiotensin, K⁺, and adrenocorticotropin, as well as a number of adipocyte-derived “aldosterone-stimulating factors.” Aldosterone mediates both genomic and nongenomic effects on the heart through its interaction with the mineralocorticoid receptor (MR), which may ultimately result in adverse cardiac remodeling. In addition, aldosterone can target adipocyte-specific MRs which may enhance adipogenesis. Furthermore, elevated aldosterone binding to adipocyte MRs may modulate adiponectin production. The presence of adiponectin receptors (AdipoR1 and AdipoR2) on the cardiomyocyte and that both aldosterone and adiponectin are synthesized in the failing human heart suggest a potential for crosstalk between adiponectin and aldosterone in pathological conditions.