Related Experiment Video
Updated: Aug 19, 2026

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
Published on: May 6, 2014
Atherosclerosis and thrombosis: lessons from animal models
1Cardiovascular Research Center, CSIC/IIBB-HSCSP-UAB, Barcelona, Spain. lbmucv@cid.csic.es
Insights
Atherothrombosis, a major cause of death, involves blood clots forming on plaques. Understanding atherosclerosis and thrombosis through animal models aids in developing new treatments for this prevalent disease.
Area of Science:
- Cardiovascular Science
- Pathophysiology
- Translational Medicine
Background:
- Atherothrombosis, thrombosis on atherosclerotic lesions, is a leading cause of mortality and disability.
- Atherosclerosis is often asymptomatic until thrombotic complications arise, necessitating early-stage disease models.
- Understanding thrombus formation secondary to plaque disruption is crucial for managing acute ischemic syndromes.
Purpose of the Study:
- To review the role of experimental models in understanding atherosclerosis and thrombosis.
- To highlight the importance of valid animal models that mimic human disease progression.
- To explore how these models enhance insights into pathophysiological processes and therapeutic interventions.
Main Methods:
- Review of experimental investigations, clinical observations, and pathological findings.
- Analysis of data from various experimental animal models of vascular disease.
- Examination of the role of specific factors like platelets, lipids, and the renin-angiotensin system (RAS).
Main Results:
- Experimental models have improved understanding of vascular obstruction in atherosclerosis and thrombosis.
- Animal models have elucidated the roles of platelets, lipids, RAS, cytokines, and growth factors.
- These models have suggested potential pharmacological and surgical therapeutic strategies.
Conclusions:
- Valid experimental models are essential for studying atherosclerosis and thrombosis.
- Advances in understanding vascular biology and pathology facilitate new therapeutic strategies.
- Continued research using animal models is key to combating atherothrombosis and its complications.
Abstract:
Atherothrombosis defines the occurrence of thrombosis on atherosclerotic lesions. Atherosclerosis is the most prevalent disease of our time and its thrombotic complications are responsible for an exceedingly high number of deaths 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 syndromes. A thrombus is usually found secondary to atherosclerotic plaque disruption. Mural thrombosis, also at the site of plaque rupture, is an important mechanism in the progression of atherosclerosis even when symptoms are absent. Because atherosclerosis is a silent and asymptomatic disease until complications arise with thrombosis producing clinical symptoms, it is necessary to have models that reproduce the human disease in its early stages. Unfortunately, not all the experimental models of vascular disease have human resemblance and validity. Knowledge of the disease process and of what an experimental animal model can offer is a milestone for a successful investigation. Experimental models of vascular disease have enhanced our understanding of the pathophysiological processes leading to vascular obstruction in both spontaneous and accelerated atherosclerosis and thrombosis. Animal models have provided insight into the role of platelets, lipids, renin-angiotensin system (RAS), cytokines and growth factors in the evolution and progression of atherosclerosis and have suggested potential therapeutic interventions. Significant advances in our understanding of the vascular biology and pathology of atherosclerosis and thrombosis, and of the interactions of blood cells, lipids and proteins with the vascular wall, have allowed us to formulate new experimental hypotheses and to test therapeutic strategies, either pharmacological or surgical.

