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Updated: Aug 25, 2026

Ferric Chloride-induced Murine Thrombosis Models
Published on: September 5, 2016
Atherogenesis and thrombosis: mechanisms, pathogenesis, and therapeutic implications
1Department of Medicine, State University of New York Health Science Center, Brooklyn 11203.
Insights
Coronary heart disease (CHD) is a leading cause of death, driven by coronary atherosclerosis. Understanding atheroma development and plaque rupture offers therapeutic targets for treatment and reversal.
Area of Science:
- Cardiovascular Medicine
- Pathology
- Medical Research
Background:
- Coronary heart disease (CHD) remains a primary cause of mortality in the US, despite a significant decline in death rates.
- Coronary atherosclerosis underlies CHD, involving a complex inflammatory and proliferative response to intimal injury.
- Acute events like myocardial infarction are linked to atherosclerotic plaque rupture and thrombosis.
Purpose of the Study:
- To elucidate the pathogenic mechanisms of coronary atherosclerosis progression.
- To identify potential therapeutic strategies for managing and potentially reversing CHD.
- To understand the factors contributing to acute coronary plaque instability.
Main Methods:
- Review of the pathological processes involved in atheroma formation and progression.
- Analysis of the sequence of cellular and molecular events following arterial injury.
- Examination of the pathophysiology of plaque rupture and luminal thrombosis.
Main Results:
- Superficial intimal injury initiates a cascade leading to obstructive atheroma development.
- Chronic injury and repeated inflammatory cycles drive atheroma progression and arterial occlusion.
- Plaque rupture, potentially due to hemodynamic stress on fragile caps, precipitates acute coronary syndromes.
Conclusions:
- Therapeutic interventions targeting platelet aggregation, coagulation, and thrombosis are crucial.
- The pathogenesis of atherosclerosis suggests possibilities for arresting and reversing the disease process.
- Further research into plaque stability mechanisms is warranted to prevent acute cardiovascular events.
Abstract:
Although the mortality rate from coronary heart disease (CHD) has declined by almost 50% during the past 25 years, CHD remains the leading cause of death in the United States and is responsible for more than 500,000 deaths annually. The underlying cause of CHD is coronary atherosclerosis. Although the intact intima is highly resistant to thrombus formation, when injury occurs, even superficial, a sequence of reactions is initiated--platelet aggregation, macrophage accumulation, intimal smooth muscle proliferation, fibrous tissue proliferation, and lipid accumulation--that result in the development of obstructive atheroma. Repeat intimal injury and cycling of this process lead to continued progression of the atheroma and coronary artery occlusion. Unstable angina and acute myocardial infarction appear to result from rupture of an atherosclerotic plaque, hemorrhage into the plaque, and luminal thrombosis. The cause of plaque rupture is unknown and may result from normal hemodynamic forces when the fibrous cap of an atheroma has become severely attenuated and fragile. Based on the pathogenesis of chronic atherosclerosis and acute rapid atheroma progression, several therapeutic options become evident. These include antiplatelet, anticoagulant, and thrombolytic therapies, as well as the possibility of arrest and reversal of atherosclerosis in some patients.
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