[HTML][HTML] Proteinases in cardiovascular aneurysms and rupture: targets for therapy?
P Carmeliet - The Journal of clinical investigation, 2000 - Am Soc Clin Investig
The Journal of clinical investigation, 2000•Am Soc Clin Investig
Figure 1 (a) Proteinase inhibitors predominate in the quiescent vessel, while net proteolysis
degrades the media and causes aneurysmal rupture during atherosclerosis. EC, endothelial
cell; SMC, smooth muscle cell; Mφ, macrophage; EL, elastic lamina.(b) Inflammatory cells
produce plasminogen (Plg) activators that activate plasmin, which degrades fibrin, laminin,
and fibronectin. By activating zymogen pro-MMPs, plasmin orchestrates degradation of
collagen and elastin, leading to complete destruction of all vessel wall matrix components.
degrades the media and causes aneurysmal rupture during atherosclerosis. EC, endothelial
cell; SMC, smooth muscle cell; Mφ, macrophage; EL, elastic lamina.(b) Inflammatory cells
produce plasminogen (Plg) activators that activate plasmin, which degrades fibrin, laminin,
and fibronectin. By activating zymogen pro-MMPs, plasmin orchestrates degradation of
collagen and elastin, leading to complete destruction of all vessel wall matrix components.
Figure 1 (a) Proteinase inhibitors predominate in the quiescent vessel, while net proteolysis degrades the media and causes aneurysmal rupture during atherosclerosis. EC, endothelial cell; SMC, smooth muscle cell; Mφ, macrophage; EL, elastic lamina.(b) Inflammatory cells produce plasminogen (Plg) activators that activate plasmin, which degrades fibrin, laminin, and fibronectin. By activating zymogen pro-MMPs, plasmin orchestrates degradation of collagen and elastin, leading to complete destruction of all vessel wall matrix components.
The Journal of Clinical Investigation