Atherosclerosis

Repairing endothelial damage could have potential relevance to reducing heart attacks, strokes, and other major causes of mortality and aging-related decline. The article distinguishes hard calcified plaque from soft plaque because they differ in stability and acute danger. A triglyceride-to-HDL ratio above 3.5 is a surrogate marker for the presence of small dense LDL particles. Different plaque types require different detection methods and imply different levels of immediate danger. Visceral fat contributes to atherosclerosis through three simultaneous pathways: a free fatty acid flood into the liver, a shift toward more dangerous LDL particle types, and insulin resistance. The article frames atherosclerosis as driven by immune dysfunction, chronic inflammation, and oxidative stress rather than cholesterol alone. Oxidized LDL particles initiate plaque formation by triggering macrophage uptake and foam cell formation. Macrophages that consume oxidized LDL become foam cells, which accumulate and form the core of atherosclerotic plaque. Foam cell clusters accumulate in the arterial wall and form early fatty streaks that can become mature plaque. VLDL produced by the liver is a precu…