The DOI matches its Crossref record; 52 of the 52 references it cites were found in a registry or an index.
Defects in caveolin-1 cause dilated cardiomyopathy and pulmonary hypertension in knockout mice
Open accessAbstract
Caveolins are important components of caveolae, which have been implicated in vesicular trafficking and signal transduction. To investigate the in vivo significance of Caveolins in mammals, we generated mice deficient in the caveolin-1 ( cav-1 ) gene and have shown that, in the absence of Cav-1, no caveolae structures were observed in several nonmuscle cell types. Although cav-1 −/− mice are viable, histological examination and echocardiography identified a spectrum of characteristics of dilated cardiomyopathy in the left ventricular chamber of the cav-1 -deficient hearts, including an enlarged ventricular chamber diameter, thin posterior wall, and decreased contractility. These animals also have marked right ventricular hypertrophy, suggesting a chronic increase in pulmonary artery pressure. Direct measurement of pulmonary artery pressure and histological analysis revealed that the cav-1 −/− mice exhibit pulmonary hypertension, which may contribute to the right ventricle hypertrophy. In addition, the loss of Cav-1 leads to a dramatic increase in systemic NO levels. Our studies provided in vivo evidence that cav-1 is essential for the control of systemic NO levels and normal cardiopulmonary function.
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Cites
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Hypertension in mice lacking the gene for endothelial nitric oxide synthase
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Loss of Caveolae, Vascular Dysfunction, and Pulmonary Defects in Caveolin-1 Gene-Disrupted Mice
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Caveolin-1 Null Mice Are Viable but Show Evidence of Hyperproliferative and Vascular Abnormalities
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Cited by
Goetz, J. G., Minguet, S., Navarro-Lérida, I., Lazcano, J. J., Samaniego, R., Calvo, E., Tello, M., Osteso-Ibáñez, T., Pellinen, T., Echarri, A., et al. (2011) · Cell · doi:10.1016/j.cell.2011.05.040 · Cited by 720
Meta-analysis identifies six new susceptibility loci for atrial fibrillation
Ellinor, P. T., Lunetta, K. L., Albert, C. M., Glazer, N. L., Ritchie, M. D., Smith, A. V., Arking, D. E., Müller-Nurasyid, M., Krijthe, B. P., Lubitz, S. A., et al. (2012) · Nature Genetics · doi:10.1038/ng.2261 · Cited by 601
Self-citationGenome-wide association study of PR interval
Pfeufer, A., van Noord, C., Marciante, K. D., Arking, D. E., Larson, M. G., Smith, A. V., Tarasov, K. V., Müller, M., Sotoodehnia, N., Sinner, M. F., et al. (2010) · Nature Genetics · doi:10.1038/ng.517 · Cited by 438
Chen, Z.-H., Lam, H. C., Jin, Y., Kim, H.-P., Cao, J., Lee, S.-J., Ifedigbo, E., Parameswaran, H., Ryter, S. W., & Choi, A. M. K. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1005574107 · Cited by 380
Endothelial cells in the pathogenesis of pulmonary arterial hypertension
Evans, C. E., Cober, N. D., Dai, Z., Stewart, D. J., & Zhao, Y.-Y. (2021) · European Respiratory Journal · doi:10.1183/13993003.03957-2020 · Cited by 325
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Metadata
- Authors
- Zhao, Y.-Y., Liu, Y., Stan, R.-V., Fan, L., Gu, Y., Dalton, N., Chu, P.-H., Peterson, K., Ross, J., & Chien, K. R.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2002-08-12
- Volume
- 99
- Issue
- 17
- Pages
- 11375-11380
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2091638984
- Cited by
- 448
- References
- 52
- FWCI
- 6.40
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Zhao, Y.-Y., Liu, Y., Stan, R.-V., Fan, L., Gu, Y., Dalton, N., Chu, P.-H., Peterson, K., Ross, J., & Chien, K. R. (2002). Defects in caveolin-1 cause dilated cardiomyopathy and pulmonary hypertension in knockout mice. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.172360799
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