Year: 2001
Type: editorial
Abstract: 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.
Source: Circulation
Authors: Peter Libby, Daniel I. Simon
Institution: Brigham and Women's Hospital
Language: English
Subfield: Hematology
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
OpenAlex ID: W2160613916