Atherosclerosis can be reversed by the clearance of cholesterol-involved foamy macrophages from the arterial intima. A recent experimental study by Park and colleagues showed that these foam-like cells are affected by interactions with oxidized low-density lipoprotein (LDL) and can migrate again after exposure to important antioxidants, such as resveratrol. Alcohols, antioxidants, are polyphenol compounds found in grapes and red wine and have the potential to fight atherosclerosis. Atherosclerosis was once thought to be a disease of fat storage -- lesions or plaques that cause artery blockage -- that results from the accumulation of fat in the arteries. The nature of atherosclerotic damage is now thought to be more complex. It manifests as localized inflammation of the vessel wall, with many local markers of chronic inflammation, including the presence of macrophages, dendritic cells, and lymphocytes. These leukocytes accumulate in specific localized areas where the underlying endothelial cells exhibit an activated or inflammatory phenotype. The initial manifestation of the lesions is fat streaks, which develop into pathological lesions under the dual influence of genes and lifestyle. The vast majority of plaques are the result of years of asymmetric disease progression, and the final obstructive event often occurs in the form of sudden embolism. Throughout the life cycle of the lesion, and during much of the period between liposteae and final disease formation, multiple events can occur that accelerate, delay, and even reverse the progression of the lesion. Chronic inflammation of the arterial wall, as a major component of atherosclerotic lesions, raises questions about the relationship between inflammation and disease extent. Inflammation is the body's normal response to trauma or infection to keep the body stable. Usually, it is self-limiting and restores tissue stability. Chronic inflammation occurs when the inflammatory response fails to resolve the event that triggered the inflammation or when self-limiting mechanisms are disrupted. Some factors that promote atherosclerosis include hyperlipidemia, lipid oxidation, leukocyte accumulation in the arterial wall, and the formation of macrophage-derived foam-like cells (Figure 1). The production of bioactive oxidized lipids in the body can trigger and regulate such inflammatory cellular events. Local accumulation of cholesterol in lesions (in the form of macrophage-derived foam cells) is hypothesized to result from excretion of key lipids, reduced activity of catalytic mechanisms, or both. At the molecular level, clearance receptors on the surface of macrophages play a key role in the formation of foam cells. For example, CD36 mediates cellular uptake of oxidized LDL by recognizing its specific truncated fatty acid moiety and oxidized phosphatidylcholine. Consistent with this observation, CD36 was found to be deficient in atherosclerosis-resistant hyperlipidemic mice. Bioactive lipids from oxidized LDL that are internalized by CD36 are able to activate nuclear receptors such as Peroxidase proliferator activates receptor gamma, thereby initiating a transcriptional program that upregulates CD36 expression, as well as the expression of other genes related to lipid metabolism. CD36 is also a direct signaling molecule; it initiates key signaling cascades. In their recent study, Park et al. describe a novel function of CD36: a regulator of cell migration. Intimal macrophage involvement contributes to lesion progression, whereas removal of macrophages from the intima promotes healing (Figure 1). Macrophage movement involves the formation of lamellipodia (protrusions from the cytoskeleton made of intracellular actin), the breakage of established local adherens junctions, and the formation of new junctions. These processes in turn rely on dynamic control of the actin cytoskeleton and local adhesion. Park et al. found that CD36 signaling caused by oxidized LDL (non-LDL) promoted actin multimerization and "firm" adhesion of cells, thus localizing foamy macrophages to the lesion. They found that CD36 signaling activates this cell colonization process through the generation of reactive oxygen species (ROS), which indirectly activates local adhesion kinases and leads to increased levels of actin polymerization. The imbalance between reactive oxygen species (ROS) and antioxidant synthesis is described as oxidative stress. ROS production in the body is counteracted by several antioxidant mechanisms. The first mechanism is the production process itself.

NADPH oxidase is the enzyme responsible for ROS production, and inhibition of this enzyme provides an attractive therapeutic direction for a variety of diseases. The second direction is antioxidants, although an effect that is sometimes insufficient to deal with ROS. Park et al. used inhibitors of two oxidases, apocynin and diphenyleneiodonium, and therapeutic doses of the antioxidants N-acetylcysteine ??and resveratrol to inhibit ROS production by macrophages in vitro. In the presence of oxidized LDL, cell migration was subsequently restored, allowing the foam cells to break free from local adhesion - a requirement for cell spreading. The antioxidants used by Park et al., which also include other antioxidants, may provide a therapeutic strategy for the treatment of atherosclerosis by reducing the adhesion and diffusion of macrophage-derived foam cells in the intima. . This reversal of the non-migratory nature of macrophages would allow foam cells to become mobile, which is necessary for cell expulsion and lesion regression. Interested comrades will discuss atherosclerosis together. Surgery cannot prevent the vein graft from hardening again. Therefore, this disease may require a breakthrough in basic science.