Figure 4. Summary of different pathways leading to increased proliferation and function of cortisol-synthesizing cells in the adrenal cortex.

Factors associated with increased activity are shown in red and include excess ACTH stimulating the MC2R (see Fig. 3). Other ACTH-independent causes include expression of receptors to other secretagogues, activating mutation of the G-protein subunit Gs-alpha, inactivating mutations of phosphodiesterases PDE8B or 11, a mutation of PRKAR1A (Carney complex), and mutations in protein kinase A catalytic subunit PRKACA. Reproduced with permission from Kirschner (2014).