Abstract
Fibrin is a major component of many atherosclerotic plaques. Within the intima there is continuous formation of fibrin, and continuous fibrinolysis. In aortic lesions, a lipoprotein bound to fibrin can be released by incubation with plasmin. Most of this lipoprotein is accounted for by Lp(a). The atherogenicity of Lp(a) may be more associated with lipid deposition than with inhibition of fibrinolysis. Fibrin degradation products may be chemotactic to monocyte-macrophages and stimulate smooth muscle cell proliferation.
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Smith, E.B., Thompson, W.D., Crosbie, L. et al. Fibrinogen/fibrin in atherogenesis. Eur J Epidemiol 8 (Suppl 1), 83–87 (1992). https://doi.org/10.1007/BF00145356
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DOI: https://doi.org/10.1007/BF00145356