Atherosclerosis and thrombosis: Lessons from animal models

Authors
Citation
L. Badimon, Atherosclerosis and thrombosis: Lessons from animal models, THROMB HAEM, 86(1), 2001, pp. 356-365
Citations number
127
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
THROMBOSIS AND HAEMOSTASIS
ISSN journal
03406245 → ACNP
Volume
86
Issue
1
Year of publication
2001
Pages
356 - 365
Database
ISI
SICI code
0340-6245(200107)86:1<356:AATLFA>2.0.ZU;2-G
Abstract
Atherothrombosis defines the occurrence of thrombosis on atherosclerotic le sions. Atherosclerosis is the most prevalent disease of our time and its th rombotic complications are responsible for an exceedingly high number of de aths and disabilities. Over the past few years, experimental investigation and clinical and pathologic observations have led to a better understanding of how a thrombus forms and also of its incidence in acute ischemic syndro mes. A thrombus is usually found secondary to atherosclerotic plaque disrup tion. Mural thrombosis, also at the site of plaque rupture, is an important mechanism in the progression of atherosclerosis even when symptoms are abs ent. Because atherosclerosis is a silent and asymptomatic disease until com plications arise with thrombosis producing clinical symptoms, it is necessa ry to have models that reproduce the human disease in its early stages. Unf ortunately, not all the experimental models of vascular disease have human resemblance and validity. Knowledge of the disease process and of what an e xperimental animal model can offer is a milestone for a successful investig ation. Experimental models of vascular disease have enhanced our understand ing of the pathophysiological processes leading to vascular obstruction in both spontaneous and accelerated atherosclerosis and thrombosis. Animal mod els have provided insight into the role of platelets, lipids, renin-angiote nsin system (RAS), cytokines and growth factors in the evolution and progre ssion of atherosclerosis and have suggested potential therapeutic intervent ions. Significant advances in our understanding of the vascular biology and pathology of atherosclerosis and thrombosis, and of the interactions of bl ood cells, lipids and proteins with the vascular wall, have allowed us to f ormulate new experimental hypotheses and to test therapeutic strategies, ei ther pharmacological or surgical.