Metalloproteinases and vulnerable atherosclerotic plaques.
Plaque rupture is the main cause of myocardial infarctions and strokes. Ruptured plaques have thin, highly inflamed, and collagen-poor fibrous caps that contain elevated levels of proteases, including metalloproteinases (MMPs), which might weaken plaque caps and promote rupture. On the other hand, MMPs facilitate migration and proliferation vascular smooth muscle cells, which should promote fibrous cap stability. Given the dual effects of MMPs, therapies should selectively target harmful MMPs or the processes that cause MMP activity to rise to destructive levels.
Newby
Andrew C
AC
University of Bristol, Bristol Heart Institute, Bristol Royal Infirmary, Bristol BS2 8HW. a.newby@bris.ac.uk
D001161:Arteriosclerosis / Q000378:metabolism* / Q000503:physiopathology; D004727:Endothelium / Q000503:physiopathology; D005109:Extracellular Matrix; D006801:Humans; D008264:Macrophages; D045726:Metalloproteases / Q000378:metabolism*; D009000:Monocytes
D045726:Metalloproteases