| Autor: |
Gomez-Arroyo JG; Victoria Johnson Center for Obstructive Lung Disease Research, Virginia Commonwealth University, Richmond, 23298, USA., Farkas L, Alhussaini AA, Farkas D, Kraskauskas D, Voelkel NF, Bogaard HJ |
| Jazyk: |
angličtina |
| Zdroj: |
American journal of physiology. Lung cellular and molecular physiology [Am J Physiol Lung Cell Mol Physiol] 2012 Feb 15; Vol. 302 (4), pp. L363-9. Date of Electronic Publication: 2011 Sep 30. |
| DOI: |
10.1152/ajplung.00212.2011 |
| Abstrakt: |
Severe forms of pulmonary arterial hypertension (PAH) are characterized by various degrees of remodeling of the pulmonary arterial vessels, which increases the pulmonary vascular resistance and right ventricular afterload, thus contributing to the development of right ventricle dysfunction and failure. Recent years have seen advances in the understanding of the pathobiology of PAH; however, many important questions remain unanswered. Elucidating the pathobiology of PAH continues to be critical to design new effective therapeutic strategies, and appropriate animal models of PAH are necessary to achieve the task. Although the monocrotaline rat model of PAH has contributed to a better understanding of vascular remodeling in pulmonary hypertension, we question the validity of this model as a preclinically relevant model of severe plexogenic PAH. Here we review pertinent publications that either have been forgotten or ignored, and we reexamine the monocrotaline model in the context of human forms of PAH. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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