A | Angiotensin II (also induces PKC-β isoform) Amylin (hyperamylinemia) / amyloid toxicity AGEs/AFEs (advanced glycosylation/fructosylation endproducts) Apolipoprotein B Antioxidant reserve compromised Absence of antioxidant network Aging ADMA (Asymmetrical DiMethyl Arginine) |
F | Free fatty acid toxicity: Obesity toxicity: Triad |
L | Lipotoxicity – Hyperlipidemia – Obesity toxicity: Triad |
I | Insulin toxicity (endogenous hyperinsulinemia-hyperproinsulinemia) Inflammation toxicity |
G | Glucotoxicity (compounds peripheral insulin resistance) reductive stress Sorbitol/polyol pathway Pseudohypoxia (increased NADH/NAD ratio) |
H | Hypertension toxicity Homocysteine toxicity hs-CRP |
T | Triglyceride toxicity: Obesity toxicity: Triad |
U | Uric Acid toxicity: Antioxidant early in physiological range and a conditional prooxidant late when elevated through the paradoxical (antioxidant → prooxidant) |
 | URATE REDOX SHUTTLE |
 | Endothelial cell dysfunction with eNOS uncoupling, decreased eNO and increased ROS. |
 | Vulnerable atherosclerotic plaque milieu of being acidic, proinflammatory, excess metal ions (Fe) (Cu) from vasa vasorum rupture and red blood cell plasma membranes due to intraplaque hemorrhage and plaque thrombus formation. |