Influence of short-term rosuvastatin therapy on endothelial progenitor cells and endothelial function
Abstract
Endothelial progenitor cells maintain endothelium integrity by replacing injured endothelial cells. Cholesterol-lowering promotes either endothelial progenitor cells mobilization or improves endothelial function. It is unknown whether improving endothelial function with statin is associated with a parallel increased endothelial progenitor cells availability. Thirty-two hypercholesterolemic patients were assigned to 4-week rosuvastatin (10 mg daily) and 16 hypercholesterolemic served as controls. Circulating endothelial progenitor cells, brachial artery flow-mediated vasodilatation, an index of endothelial function, and the lipid profile were measured before and after the 4-week statin therapy. At baseline, we found a correlation between circulating endothelial progenitor cells and flow-mediated vasodilatation (r = .31, P = .029). At the end of the 4-week intervention with rosuvastatin there was a 37% reduction in low-density lipoprotein cholesterol (P < .001) and a significant 72% increase in the number of endothelial progenitor cells and flow-mediated vasodilatation (4.7 + 0.7% to 8.8 + 0.4%, P < .001). Endothelial progenitor cells and flow-mediated vasodilatation were unchanged at the end of the study in patients not taking statin. A correlation emerged between endothelial progenitor cells and flow-mediated vasodilatation variations (r = .52, P < .001), this correlation being still significant after controlling for blood cholesterol reduction. In conclusion, short-term rosuvastatin therapy contributes in hyperchoelsterolemic patients to improving endothelial function by lowering cholesterol and increasing the number of circulating endothelial progenitor cells; the latter effect appears to be partly independent from reduction in plasma cholesterol.
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Cholesterol-lowering attenuation of inflammation may positively influence vascular injury and cardiovascular prognosis.
“Hence, it is believed that attenuation of inflammation by cholesterol lowering may have a positive influence on vascular injury (151) and CV prognosis (152).”
From The Role of Nutraceuticals in Statin Intolerant Patients (2018) · cites this paper as [151]
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Плейотропні ефекти статинів: більше ніж просто зниження холестерину
Kanishcheva, O., Tselik, N. E., Lebedynska, M. M., & Shop, I. V. (2026) · Ukrainian Journal of Cardiology · doi:10.31928/2664-4479-2026.3.4656
- Authors
- Pirro, M., Schillaci, G., Romagno, P. F., Mannarino, M. R., Bagaglia, F., Razzi, R., Pasqualini, L., Vaudo, G., & Mannarino, E.
- Affiliations
- University of Perugia (IT)
- Corresponding author
- Pirro, Matteo
- Venue
- Journal of Cardiovascular Pharmacology and Therapeutics
- Publisher
- SAGE Publications
- Published
- 2009-03
- Volume
- 14
- Issue
- 1
- Pages
- 14-21
- ISSN
- 1074-2484 (ISSN-L)
- 1940-4034
- OpenAlex
- W2113841285
- Cited by
- 64
- References
- 27
- Citations by year
- 2026: 2 · 2023: 6 · 2022: 5 · 2021: 6 · 2019: 1 · 2018: 8 · 2017: 8 · 2016: 2 · 2015: 2 · 2014: 2 · 2013: 4 · 2012: 5
- FWCI
- 6.05
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Cardiovascular Pharmacology and Therapeutics (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Fondazione Cassa di Risparmio di Perugia
- Topics
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Keywords
- rosuvastatin, endothelial progenitor cells, endothelial function, flow-mediated dilation, hypercholesterolemia, statins, LDL cholesterol lowering, brachial artery, lipid profile
- MeSH terms
- Rosuvastatin Calcium, Cholesterol, Drug Administration Schedule, Endothelium, Vascular, Female, Fluorobenzenes, Humans, Hypercholesterolemia, Male, Middle Aged, Prospective Studies, Pyrimidines, Stem Cells, Sulfonamides, Vasodilation, Treatment Outcome, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Endothelial Cells
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