The DOI matches its Crossref record; 58 of the 58 references it cites were found in a registry or an index.
Pulmonary Arterial Hypertension Is Linked to Insulin Resistance and Reversed by Peroxisome Proliferator–Activated Receptor-γ Activation
Abstract
Background— Patients with pulmonary arterial hypertension (PAH) have reduced expression of apolipoprotein E (apoE) and peroxisome proliferator–activated receptor-γ in lung tissues, and deficiency of both has been linked to insulin resistance. ApoE deficiency leads to enhanced platelet-derived growth factor signaling, which is important in the pathobiology of PAH. We therefore hypothesized that insulin-resistant apoE-deficient (apoE −/− ) mice would develop PAH that could be reversed by a peroxisome proliferator–activated receptor-γ agonist (eg, rosiglitazone). Methods and Results— We report that apoE −/− mice on a high-fat diet develop PAH as judged by elevated right ventricular systolic pressure. Compared with females, male apoE −/− were insulin resistant, had lower plasma adiponectin, and had higher right ventricular systolic pressure associated with right ventricular hypertrophy and increased peripheral pulmonary artery muscularization. Because male apoE −/− mice were insulin resistant and had more severe PAH than female apoE −/− mice, we treated them with rosiglitazone for 4 and 10 weeks. This treatment resulted in markedly higher plasma adiponectin, improved insulin sensitivity, and complete regression of PAH, right ventricular hypertrophy, and abnormal pulmonary artery muscularization in male apoE −/− mice. We further show that recombinant apoE and adiponectin suppress platelet-derived growth factor-BB–mediated proliferation of pulmonary artery smooth muscle cells harvested from apoE −/− or C57Bl/6 control mice. Conclusions— We have shown that insulin resistance, low plasma adiponectin levels, and deficiency of apoE may be risk factors for PAH and that peroxisome proliferator–activated receptor-γ activation can reverse PAH in an animal model.
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Cites
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Expression of Endothelin-1 in the Lungs of Patients with Pulmonary Hypertension
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Cited by
Mechanisms of disease: pulmonary arterial hypertension
Schermuly, R. T., Ghofrani, H. A., Wilkins, M. R., & Grimminger, F. (2011) · Nature Reviews Cardiology · doi:10.1038/nrcardio.2011.87 · Cited by 800
Archer, S. L., Weir, E. K., & Wilkins, M. R. (2010) · Circulation · doi:10.1161/circulationaha.108.847707 · Cited by 485
Hansmann, G., de Jesus Perez, V. A., Alastalo, T.-P., Alvira, C. M., Guignabert, C., Bekker, J. M., Schellong, S., Urashima, T., Wang, L., Morrell, N. W., et al. (2008) · Journal of Clinical Investigation · doi:10.1172/jci32503 · Cited by 367
Self-citationArcher, S. L., Gomberg-Maitland, M., Maitland, M. L., Rich, S., Garcia, J. G. N., & Weir, E. K. (2008) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.01324.2007 · Cited by 366
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
- Hansmann, G., Wagner, R. A., Schellong, S., de Jesus Perez, V. A., Urashima, T., Wang, L., Sheikh, A. Y., Suen, R. S., Stewart, D. J., & Rabinovitch, M.
- Venue
- Circulation
- Published
- 2007-03-13
- Volume
- 115
- Issue
- 10
- Pages
- 1275-1284
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2088829415
- Cited by
- 366
- References
- 58
- FWCI
- 15.62
- Type
- journal article
- Language
- en
- Open access
- closed
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- Hansmann, G., Wagner, R. A., Schellong, S., de Jesus Perez, V. A., Urashima, T., Wang, L., Sheikh, A. Y., Suen, R. S., Stewart, D. J., & Rabinovitch, M. (2007). Pulmonary Arterial Hypertension Is Linked to Insulin Resistance and Reversed by Peroxisome Proliferator–Activated Receptor-γ Activation. Circulation. https://doi.org/10.1161/circulationaha.106.663120
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