Table 9 Courtesy [8, 9, 53] The RAAS acronym: for the prevention and treatment of redox stress in atheroscleropathy and stablization of the vulnerable intima and islet in T2DM

Reductase inhibitors (HMG-CoA). Decreasing modified LDL cholesterol, i.e. oxidized, acetylated LDL cholesterol. Improving endothelial cell dysfunction. Thus, decreasing the oxidative stress to the arterial vessel wall and the islet. Redox stress reduction.

ACEi-prils. ARBS-sartans. Both inhibiting the effect of angiotensin-II locally as well as systemically. Affecting hemodynamic stress through their antihypertensive effect as well as the deleterious effects of angiotensin II on cells at the local level – injurious stimuli. Decreasing the A-FLIGHT toxicities. Plus the direct/indirect antioxidant effect within the islet and the arterial vessel wall. Redox stress reduction.

Aspirin antiplatelet, anti-inflammatory effect.

Aggressive control of diabetes. Decreasing modified LDL cholesterol, i.e. glycated LDL cholesterol. Improving endothelial cell dysfunction. Also decreasing glucose toxicity and the redox stress to the intima and pancreatic islet. Aggressive control of Hcy with folic acid with its associated additional positive effect on re-coupling of the BH4 cofactor with the eNOS reaction to produce eNO. Redox stress reduction.

Statins. Improving plaque stability (pleiotropic effects) independent of cholesterol lowering. Improving endothelial cell dysfunction and preventing the angiogenesis associated with arterial vascular remodeling which destabilizes the unstable atherosclerotic plaque. Plus, the direct/indirect antioxidant anti-inflammatory effects within the islet and the arterial vessel wall promoting stabilization of the unstable, vulnerable islet and the arterial vessel wall. Style: Lifestyle modification: Stop smoking, lose weight, exercise, and change eating habits. Redox stress reduction