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Why does endothelial injury encourage plaque formation in an artery?
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cardiovascular disease
This micrograph shows a cross section of a coronary artery narrowed by an atherosclerotic plaque (purplish matter inside the artery). Most heart attacks are caused by the rupture of an atherosclerotic plaque, which triggers the formation of a clot that abruptly blocks blood flow to part of the heart muscle.
Endothelial injury is a critical initiating event in the development of atherosclerosis. When the inner lining of an artery is damagedāoften by factors such as high cholesterol, high blood pressure, or tobacco smokeāit triggers a complex inflammatory response that encourages plaque formation.1
The process unfolds through several key mechanisms:
- Cellular Recruitment: Injury to the endothelium causes platelets and monocytes to adhere to the damaged site. These cells release chemical signals that attract additional cells to the area.21
- Lipid Accumulation: The damaged endothelium becomes more permeable, allowing low-density lipoproteins (LDLs) to infiltrate the arterial wall. Macrophages are drawn to the site to scavenge these lipids, becoming lipid-filled "foam cells" that eventually die and accumulate.32
- Plaque Growth: Over time, a mixture of foam cells, cellular debris, calcium, and smooth muscle cells builds up, while the production of connective tissue further thickens the lesion. This mass forms an atheroma, or atherosclerotic plaque, which narrows the arterial lumen and restricts blood flow.31