A Culprit Cell that Drives Plaque Buildup in Arteries (IMAGE)
Caption
Shown is a cross section through an atherosclerotic plaque of an LDLR knockout mouse fed a high fat diet for 12 weeks. The plaque is stained for senescence-associated beta galactosidase to visualize senescent (often referred to as "zombie") cells. Our research shows that these cells are present throughout plaque development. We find that at the earliest stages of disease, senescent cells propel plaque emlargement through the secretion of factors that attract circulating monocytes to the plaque. At advanced disease stages, senescent cells produce enzymes that dissolve the fibrous cap that overlays the plaque to give it stability, thereby promoting plaque rupture, coagulation of platelets at the site of rupture, full arterial occlusion and myocardial infarction. We show that drugs that eliminate senescent cells (referred to senolytics) inhibit plaque expansion and preserve the cap, giving plaques long-term stability.
Credit
Jan van Deursen and Bennett Childs
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