The DOI matches its Crossref record; 138 of the 138 references it cites were found in a registry or an index.
Animal models of pulmonary arterial hypertension: the hope for etiological discovery and pharmacological cure
Abstract
At present, six groups of chronic pulmonary hypertension (PH) are described. Among these, group 1 (and 1′) comprises a group of diverse diseases termed pulmonary arterial hypertension (PAH) that have several pathophysiological, histological, and prognostic features in common. PAH is a particularly severe and progressive form of PH that frequently leads to right heart failure and premature death. The diagnosis of PAH must include a series of defined clinical parameters, which extend beyond mere elevations in pulmonary arterial pressures and include precapillary PH, pulmonary hypertensive arteriopathy (usually with plexiform lesions), slow clinical onset (months or years), and a chronic time course (years) characterized by progressive deterioration. What appears to distinguish PAH from other forms of PH is the severity of the arteriopathy observed, the defining characteristic of which is “plexogenic arteriopathy.” The pathogenesis of this arteriopathy remains unclear despite intense investigation in a variety of animal model systems. The most commonly used animal models (“classic” models) are rodents exposed to either hypoxia or monocrotaline. Newer models, which involve modification of classic approaches, have been developed that exhibit more severe PH and vascular lesions, which include neointimal proliferation and occlusion of small vessels. In addition, genetically manipulated mice have been generated that have provided insight into the role of specific molecules in the pulmonary hypertensive process. Unfortunately, at present, there is no perfect preclinical model that completely recapitulates human PAH. All models, however, have provided and will continue to provide invaluable insight into the numerous pathways that contribute to the development and maintenance of PH. Use of both classic and newly developed animal models will allow continued rigorous testing of new hypotheses regarding pathogenesis and treatment. This review highlights progress that has been made in animal modeling of this important human condition.
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1 retracted
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RetractedUpdated clinical classification of pulmonary hypertension
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Cited by
Burgstaller, G., Oehrle, B., Gerckens, M., White, E. S., Schiller, H. B., & Eickelberg, O. (2017) · European Respiratory Journal · doi:10.1183/13993003.01805-2016 · Cited by 482
Cellular senescence impairs the reversibility of pulmonary arterial hypertension
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The Fra-2 transgenic mouse model of systemic sclerosis
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HIF-2α is essential for carotid body development and function
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Redox regulation of responses to hypoxia and NO–cGMP signaling in pulmonary vascular pathophysiology
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Metadata
- Authors
- Stenmark, K. R., Meyrick, B., Galie, N., Mooi, W. J., & McMurtry, I. F.
- Venue
- American Journal of Physiology-Lung Cellular and Molecular Physiology
- Publisher
- American Physiological Society
- Published
- 2009-12
- Volume
- 297
- Issue
- 6
- Pages
- L1013-L1032
- ISSN
- 1040-0605 (ISSN-L)
- 1522-1504
- OpenAlex
- W2136978968
- Cited by
- 774
- References
- 138
- FWCI
- 36.34
- Type
- journal article
- Language
- en
- Open access
- closed
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- Stenmark, K. R., Meyrick, B., Galie, N., Mooi, W. J., & McMurtry, I. F. (2009). Animal models of pulmonary arterial hypertension: the hope for etiological discovery and pharmacological cure. American Journal of Physiology-Lung Cellular and Molecular Physiology. https://doi.org/10.1152/ajplung.00217.2009
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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