Role and Mechanism of the Renin-Angiotensin-Aldosterone System in the Onset and Development of Cardiorenal Syndrome

Figure 2

Schematic representation of RAAS-mediated CRS. ① RAAS-mediated oxidative stress not only increases the preload and afterload of the heart by inducing renal fibrosis and atherosclerosis, respectively, but also induces cardiac fibrosis, which further leads to cardiac dysfunction, reduced circulating blood volume, and ultimately renal insufficiency. ② FGF-23 alters the functional activities of the heart by inducing atrial fibrillation, left ventricular hypertrophy, and cardiac fibrosis. PBUT not only causes endothelial dysfunction but also induces cardiac dysfunction by inducing cardiomyocyte fibrosis and apoptosis. ③ RAAS-mediated ADMA production induces endothelial dysfunction by reducing NO production. Endothelial dysfunction increases cardiac preload by reducing the glomerular filtration rate, further leading to cardiac dysfunction.