The DOI matches its Crossref record; 34 of the 34 references it cites were found in a registry or an index.
Accelerated Atherosclerosis, Aortic Aneurysm Formation, and Ischemic Heart Disease in Apolipoprotein E/Endothelial Nitric Oxide Synthase Double-Knockout Mice
Abstract
Background To test whether deficiency in endothelial nitric oxide synthase (eNOS) affects atherosclerosis development, we compared lesion formation in apolipoprotein E (apoE)/eNOS-double knockout (DKO) and apoE-knockout (KO) control animals. Methods and Results After 16 weeks of “Western-type” diet, apoE/eNOS-DKO males and females showed significant increases in lesion area of 93.6% and 59.2% compared with apoE-KO mice. All apoE/eNOS-DKO animals studied developed peripheral coronary arteriosclerosis, associated with perivascular and myocardial fibrosis, whereas none of the apoE-KO mice did. Transthoracic echocardiography showed a significantly increased left ventricular wall thickness and decreased fractional shortening in DKO animals. Mean arterial pressure was increased in DKO mice and was comparable in degree to eNOS-KO animals. Male DKO animals developed atherosclerotic abdominal aneurysms and aortic dissection. Conclusions eNOS deficiency increases atherosclerosis in Western-type diet-fed apoE-KO animals and introduces coronary disease and an array of cardiovascular complications, including spontaneous aortic aneurysm and dissection. This phenotype constitutes the first murine model to demonstrate distal coronary arteriosclerosis associated with evidence of myocardial ischemia, infarction, and heart failure. Hypertrophy and reduced left ventricular function cannot be explained by increased blood pressure alone, because eNOS-KO animals do not develop these complications.
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Cited by
The Pathobiology of Diabetic Complications
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Roles of vascular oxidative stress and nitric oxide in the pathogenesis of atherosclerosis
Förstermann, U., Xia, N., & Li, H. (2017) · Circulation Research · doi:10.1161/circresaha.116.309326 · Cited by 1,519
Mouse Models of Diabetic Nephropathy
Brosius, F. C., Alpers, C. E., Bottinger, E. P., Breyer, M. D., Coffman, T. M., Gurley, S. B., Harris, R. C., Kakoki, M., Kretzler, M., Leiter, E. H., et al. (2009) · Journal of the American Society of Nephrology · doi:10.1681/asn.2009070721 · Cited by 895
Endothelial Function: A Critical Determinant in Atherosclerosis?
Landmesser, U., Hornig, B., & Drexler, H. (2004) · Circulation · doi:10.1161/01.cir.0000129501.88485.1f · Cited by 851
Reactive oxygen species in cardiovascular disease
Sugamura, K., & Keaney (2011) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2011.05.004 · Cited by 769
Metadata
- Authors
- Kuhlencordt, P. J., Gyurko, R., Han, F., Scherrer-Crosbie, M., Aretz, T. H., Hajjar, R., Picard, M. H., & Huang, P. L.
- Venue
- Circulation
- Published
- 2001-07-24
- Volume
- 104
- Issue
- 4
- Pages
- 448-454
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2159819574
- Cited by
- 630
- References
- 34
- FWCI
- 16.39
- Type
- journal article
- Language
- en
- Open access
- closed
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- Kuhlencordt, P. J., Gyurko, R., Han, F., Scherrer-Crosbie, M., Aretz, T. H., Hajjar, R., Picard, M. H., & Huang, P. L. (2001). Accelerated Atherosclerosis, Aortic Aneurysm Formation, and Ischemic Heart Disease in Apolipoprotein E/Endothelial Nitric Oxide Synthase Double-Knockout Mice. Circulation. https://doi.org/10.1161/hc2901.091399
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