The DOI matches its Crossref record; 56 of the 56 references it cites were found in a registry or an index.
Statin-Induced Improvement of Endothelial Progenitor Cell Mobilization, Myocardial Neovascularization, Left Ventricular Function, and Survival After Experimental Myocardial Infarction Requires Endothelial Nitric Oxide Synthase
Open accessAbstract
Background— Endothelial nitric oxide (eNO) bioavailability is severely reduced after myocardial infarction (MI) and in heart failure. Statins enhance eNO availability by both increasing eNO production and reducing NO inactivation. We therefore studied the effect of statin treatment on eNO availability after MI and tested its role for endothelial progenitor cell mobilization, myocardial neovascularization, left ventricular (LV) dysfunction, remodeling, and survival after MI. Methods and Results— Wild-type (WT) and eNO synthase (eNOS) −/− mice with extensive anterior MI were randomized to treatment with vehicle (V) or atorvastatin (Ator, 50 mg/kg QD by gavage) for 4 weeks starting on day 1 after MI. Ator markedly improved endothelium-dependent, NO-mediated vasorelaxation; mobilization of endothelial progenitor cells; and myocardial neovascularization of the infarct border in WT mice after MI while having no effect in eNOS −/− mice. LV dysfunction and interstitial fibrosis were markedly attenuated by Ator in WT mice, whereas no effect was observed in eNOS −/− mice after MI. Importantly, Ator significantly increased the survival rate during 4 weeks after MI in WT mice (Ator versus V, 80% versus 46%; P <0.01, n=75) but not in eNOS −/− mice (43% versus 48%; NS, n=42). Conclusions— These findings suggest that increased eNO availability is required for statin-induced improvement of endothelial progenitor cell mobilization, myocardial neovascularization, LV dysfunction, interstitial fibrosis, and survival after MI. eNO bioavailability after MI likely represents an important therapeutic target in heart failure after MI and mediates beneficial effects of statin treatment after MI.
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Cited by
Nitric oxide synthases: regulation and function
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Role of microRNAs in vascular diseases, inflammation, and angiogenesis
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Self-citationAging and disease as modifiers of efficacy of cell therapy
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Metadata
- Authors
- Landmesser, U., Engberding, N., Bahlmann, F. H., Schaefer, A., Wiencke, A., Heineke, A., Spiekermann, S., Hilfiker-Kleiner, D., Templin, C., Kotlarz, D., Mueller, M., Fuchs, M., Hornig, B., Haller, H., & Drexler, H.
- Venue
- Circulation
- Published
- 2004-10-05
- Volume
- 110
- Issue
- 14
- Pages
- 1933-1939
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2169937658
- Cited by
- 423
- References
- 56
- FWCI
- 18.81
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: Statin-Induced Improvement of Endothelial Progenitor Cell Mobilization, Myocardial Neovascularization, Left Ventricular Function, and Survival After Experimental Myocardial Infarction Requires Endothelial Nitric Oxide Synthase. https://app.cochat.ai/papers/10.1161/01.cir.0000143232.67642.7a
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- Landmesser, U., Engberding, N., Bahlmann, F. H., Schaefer, A., Wiencke, A., Heineke, A., Spiekermann, S., Hilfiker-Kleiner, D., Templin, C., Kotlarz, D., Mueller, M., Fuchs, M., Hornig, B., Haller, H., & Drexler, H. (2004). Statin-Induced Improvement of Endothelial Progenitor Cell Mobilization, Myocardial Neovascularization, Left Ventricular Function, and Survival After Experimental Myocardial Infarction Requires Endothelial Nitric Oxide Synthase. Circulation. https://doi.org/10.1161/01.cir.0000143232.67642.7a
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
