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[137] [138] [139] 8-oxoG, a common type of oxidative damage in DNA, is found to accumulate in plaque vascular smooth muscle cells, macrophages and endothelial cells, [140] thus linking DNA damage to plaque formation. DNA strand breaks also increased in atherosclerotic plaques. [140] Werner syndrome (WS) is a premature aging condition in humans ...
Atherosclerosis is characterized by the build-up of plaque inside your blood vessels. It can lead to stenosis, which is a narrowing of your artery walls. Plaque is a fatty substance made up of:
The link between atherosclerosis and autoimmunity is plasmacytoid dendritic cells (pDCs). PDCs contribute to the early stages of the formation of atherosclerotic lesions in the blood vessels by releasing large quantities of type 1 interferons (INF). Stimulation of pDCs leads to an increase of macrophages present in plaques.
An atheroma, or atheromatous plaque, is an abnormal accumulation of material in the inner layer of an arterial wall. [1] [2]The material consists of mostly macrophage cells, [3] [4] or debris, containing lipids, calcium and a variable amount of fibrous connective tissue.
Current research and thinking relating to the formation of vulnerable plaques (see atherosclerosis) is: [3] Hyperlipidemia, hypertension, smoking, homocysteine, hemodynamic factors, toxins, viruses, and/or immune reactions results in chronic endothelial injury, dysfunction, and increased permeability. [4]
The readouts are derived from white blood cells, including monocytes, which play key roles in atherosclerotic plaque formation and inflammation, linking directly to cardiovascular risk.
Arteriosclerosis, literally meaning "hardening of the arteries", is an umbrella term for a vascular disorder characterized by abnormal thickening, hardening, and loss of elasticity [3] of the walls of arteries; [4] this process gradually restricts the blood flow to one's organs and tissues and can lead to severe health risks brought on by atherosclerosis, which is a specific form of ...
The most frequent cause of MI is the rupturing of an atherosclerotic plaque formed in CAD. Plaque rupture exposes the subendothelial matrix beneath the plaque, initiating thrombus formation within the vasculature. [7] The thrombus deposits on the ruptured plaque to completely block the coronary artery, halting oxygen supply to cardiomyocytes.