Figure 1.

Five emerging molecular points of aldosterone–AR signaling crosstalk in the heart. 1. OPN is transcriptionally upregulated by aldosterone and, in turn, dampens the cAMP-mediated anti-fibrotic signaling of the β₂AR; 2. β₂AR-stimulated GRK5 “sheds” from the plasma membrane to the cytoplasm, wherein it phosphorylates and inhibits MR (prevents MR nuclear translocation); 3. Aldosterone enhances catecholamine (βAR)-mediated ERK activation resulting in enhanced fibrosis; 4. MR inhibits CREB (usually activated by βARs) via CLN/PP2B; 5. α₁AR-activated PKC enhances aldosterone-induced hypertrophy and adverse remodeling. Adapted from Parker at al., 2018 [3].