Atherosclerosis is the development of fatty plaques in blood vessel walls, formed of damaged lipids and the debris of dead cells. Once developed in earnest, these become localized areas of chronic inflammation. Inflammatory signaling continually calls in macrophages that attempt to clear up the damage, become overwhelmed, and add their remains to the growing mass. In the late stage of the condition, blood vessels are narrowed and weakened, and the plaques become unstable, prone to rupture. Here, researchers show that cells found in unstable fatty plaque are distinct from those in stable plaque. They look more like cancer cells or activated immune cells in the operation of their metabolism.
This is interesting in light of the recent discovery that growth and instability in atherosclerotic plaque is driven in part by the senescence of macrophages. The macrophages attempting to clean up the plaque become senescent as they are overwhelmed by damaged lipids that they cannot effectively break down. They become foam cells as they are loaded with lipids, and the foam cells become senescent in response to their own damaged state and the plaque environment. Senescent cells secrete signals that promote inflammation and disruptive remodeling of surrounding tissue structure, and are
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