This Review discusses the concept of Ras-related C3 botulinum toxin substrate 1 (Rac1)-induced activation of the mineralocorticoid receptor and highlights the available evidence for the roles of Rac1 and mineralocorticoid-receptor activation in cardiac and renal disease. The authors suggest that agents that regulate the activity of the Rac1-mineralocorticoid-receptor pathway could be novel therapeutic candidates for the treatment of chronic kidney disease and cardiac injury.
- Miki Nagase
- Toshiro Fujita
