Fig. 3.
Mechanisms by which mTOR/S6K signaling pathways mediate overnutrition-induced cardiovascular diseases in the cardiorenal syndrome (CRS). Overnutrition activates mTOR/S6K signaling pathways and renin-angiotensin-aldosterone-system (RAAS), resulting in insulin resistance, autophagic inhibition, and reduced T regulatory cell (Treg) differentiation and maturation, which promote endothelial dysfunction, arterial stiffness, hypertension, atherosclerosis, and left ventricular diastolic dysfunction. In contrast, increased ANG type 2 receptor (AT2R) activation serves as a protective feedback mechanism to balance enhanced mTORC1 signaling. EC, endothelial cell; IRS, insulin receptor substrate; MR, mineralocorticoid receptor.