An update of the Grützbalg  hypothesis: the role of thrombosis and coagulation in atherosclerotic progression.
The Grützbalg analogy has obviously held up and been greatly extended by current work implicating specific molecules in inflammation and proteolysis. Still, Virchow's explanation is only partly able to account for the chronic outcome of this disease. Many of the open questions center on fibrin. For example, we do not know why fibrin forms in Virmani's eroded lesions. If the source of tissue factor in erosion is Nemerson's "stealth" particles, we may also need to rethink the source of tissue factor in plaque rupture. At the other extreme, as we all know, atherosclerotic vascular disease is a chronic disease. While multiple episodes of plaque rupture are likely to be important in this chronic process, the critical events here--scarring, narrowing of the lumen--remain largely unexplained. The data reviewed here suggest that intramural coagulation could be a critical process underlying these chronic changes.
Department of Pathology, University of Washington, Seattle 98195-7335, USA.
K O
KO
Yee
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Ikari
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Schwartz
D000818:Animals; D001161:Arteriosclerosis / Q000097:blood / Q000209:etiology* / Q000473:pathology; D001777:Blood Coagulation / Q000502:physiology*; D018450:Disease Progression; D005337:Fibrin / Q000378:metabolism / Q000502:physiology; D006801:Humans; D008954:Models, Biological; D013927:Thrombosis / Q000150:complications / Q000473:pathology / Q000503:physiopathology*
D005337:Fibrin