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In diseases such as atherosclerosis, thrombosis involves an intricate interface with inflammation rather than acting solely as a simple protective mechanism against blood loss.
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Highlights the complex interplay between inflammation and thrombosis in the pathogenesis of atherosclerosis.
extbooks often portray thrombosis as a bland protective mechanism critical for stanching blood loss after injury: the prick of a lancet, the wound of a scalpel, or the predator's fangs neatly trigger a proteolytic cascade culminating in fibrin formation and cross-linking.However, in diseases such as atherosclerosis, the picture differs substantially from this simplistic model.In the natural history of atherosclerosis, thrombosis involves an inciting injury more subtle than a wound.In such pathological states, the importance of an intricate interface between inflammation and thrombosis becomes apparent.
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Libby et al. (2001) conducted a review in Atherosclerosis. In diseases such as atherosclerosis, thrombosis involves an intricate interface with inflammation rather than acting solely as a simple protective mechanism against blood loss.
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