Oxidation arteriosclerosis caused

Fig. 2. Proposed process of arteriosclerosis leading to ischemic disease. It is proposed that arteriosclerosis is a process of inflammation within the arterial wall that is initiated by arterial injury (endothelial dysfunction), causing the trapping of lipoproteins (Rll, Zl). These undergo oxidation as proposed in Fig. 1, leading to foam cells saturated with lipid droplets. Continued accumulation of fatty material within the blood vessel wall promotes a fatty streak. Ultimately, there is muscle cell migration and fibrosis leading to a plaque that consists of a fibrous cap with cholesterol crystals and debris within the deep necrotic layer, while inflammatory cells form a dynamic outer edge. It is thought that oxidized lipoproteins can facilitate many of these processes. Mechanical forces predispose the soft outer layer of the plaque to rupture at sites of structural weakness. Rupture of plaques causes thrombosis and incorporation of thrombi into the plaque. Ultimately, a large thrombus appearing in an obstructed vessel can lead to sudden ischemia and unstable coronary syndromes.

Although it is not yet conclusively proven that oxidation is the cause of arteriosclerosis in humans (C3, SIO), animal experiments in the form of transgenic and knockout mice models support this hypothesis (C3). OxLDL (Tsl2, Y2) and lipid oxidation products are found in human arteriosclerotic... 

Much evidence suggests that oxidation of lipoproteins is a cause of human arteriosclerosis. This comprises animal models, including those in which several different antioxidant compounds retarded arteriosclerosis, epidemiological studies (C3, SIO), and correlation between oxidation products and CAD in humans (A2, H7, J9). Moreover, evidence shows accumulations of oxidation products in human arteriosclerotic tissue and gruel. These include ... 

---