Endothelial progenitor cells in the natural history of atherosclerosis
Gian Paolo Fadini1, Carlo Agostini, Saverio Sartore
1Department of Clinical and Experimental Medicine, University of Padova, Medical School, Padova, Italy. gianpaolofadini@hotmail.com
Insights
Endothelial progenitor cells (EPCs) are crucial for repairing blood vessels and forming new ones. Alterations in EPCs play a significant role in the development and progression of atherosclerosis.
Area of Science:
- Cardiovascular Research
- Cell Biology
- Regenerative Medicine
Background:
- Atherosclerotic diseases are a leading cause of morbidity and mortality.
- Classical views attribute lesion development to inflammation following endothelial damage.
- Emerging evidence highlights the role of bone marrow-derived cells in endothelial repair.
Purpose of the Study:
- To review the role of endothelial progenitor cells (EPCs) in atherosclerosis.
- To explore how EPC alterations impact disease stages and clinical manifestations.
- To emphasize the significance of EPCs in atherogenesis.
Main Methods:
- Literature review of studies on EPCs and atherosclerosis.
- Analysis of the impact of risk factors on EPCs.
- Examination of mechanisms linking EPC dysfunction to plaque formation.
Main Results:
- Quantitative and qualitative alterations in EPCs are implicated in all stages of atherosclerosis.
- Risk factors negatively affect EPC function and number.
- Reduced or dysfunctional EPCs are linked to plaque development and clinical syndromes.
Conclusions:
- Endothelial progenitor cells (EPCs) are central to the endogenous repair of the endothelium.
- EPC dysfunction is a key factor in the pathogenesis of atherosclerosis.
- Focusing on EPCs in the bloodstream offers new insights into atherogenesis.
Abstract:
Atherosclerotic diseases are responsible for a significant part of morbidity and mortality in western countries. According to the classical views, atherosclerotic lesions develop as the result of an inflammatory process initiated by endothelial damage. The discovery that bone marrow-derived cells participate in endothelial repair and new vessel growth has changed the pathogenetic models of cardiovascular disease. These cells, termed endothelial progenitor cells (EPCs), represent the endogenous endothelial regenerative capacity and the ability to form new collateral vessels. In this review we describe how quantitative and qualitative alterations of EPCs have a significant role in virtually all stages of the atherosclerotic process and in the clinical manifestations of the diseases: starting from the impact of risk factors on EPCs, through the mechanisms that link EPC reduction/dysfunction to plaque formation, and finally to the clinical syndromes. An attempt to diverge our attention from the vessel wall to the bloodstream reveals a central role of EPCs in atherogenesis.
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