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The pathogenesis of atherosclerosis: an overview
C J Schwartz1, A J Valente, E A Sprague
1Department of Pathology, University of Texas Health Science Center, San Antonio 78284-7750.
Clinical Cardiology
|February 1, 1991
Summary
Atherosclerosis pathogenesis involves arterial inflammation and healing in hyperlipidemia, driven by low-density lipoprotein (LDL) accumulation and oxidation. Targeting LDL reduction and enhancing reverse cholesterol transport can prevent and treat this cardiovascular disease.
Area of Science:
- Cardiovascular Biology
- Pathogenesis of Atherosclerosis
- Lipid Metabolism
Background:
- Atherosclerosis is characterized by focal arterial lesions.
- Key initial events include low-density lipoprotein (LDL) influx and monocyte recruitment.
- Hyperlipidemia exacerbates these processes, overwhelming macrophage clearance mechanisms.
Purpose of the Study:
- To present a unifying hypothesis on the etiology and pathogenesis of atherosclerosis.
- To emphasize the role of focal lesion-prone sites.
- To outline potential targets for prevention and treatment.
Main Methods:
- This is a hypothesis-driven review, synthesizing existing knowledge.
- It focuses on the cellular and molecular mechanisms of lesion development.
- It discusses the role of oxidized LDL (Ox-LDL), macrophages, smooth muscle cells, and inflammatory cells.
Main Results:
- Oxidized LDL (Ox-LDL) uptake by macrophages forms foam cells.
- Necrotic extracellular lipid cores form from cell death.
- Monocyte chemoattractant protein-1 (MCP-1) regulates monocyte recruitment.
- Smooth muscle cell migration and proliferation contribute to plaque growth.
- Inflammatory cells and thrombosis play roles in advanced plaque development.
- Plaque regression involves reverse cholesterol transport.
Conclusions:
- Atherosclerosis involves arterial inflammatory and healing processes in a hyperlipidemic environment.
- Genetic, hemodynamic, and risk factors modulate pathogenesis.
- Prevention and treatment should target LDL reduction, inhibition of LDL oxidation, and augmentation of reverse cholesterol transport.