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- W216954906 endingPage "72" @default.
- W216954906 startingPage "51" @default.
- W216954906 abstract "Pulmonary arterial hypertension comprises a group of clinical and pathophysiological entities with similar features but a variety of underlying causes. Genetic polymorphisms, environmental exposures, and acquired disorders predispose patients to PAH, but none of the factors alone is sufficient to cause the disease. PAH is an end-stage phenotype that represents a final common manifestation of multiple preclinical, intermediate phenotypes. Thus, an understanding of the preclinical disease in at-risk populations will be critical for identifying the primary pathogenic mechanisms. Because clinically apparent disease occurs in only a small percentage of carriers of BMPR2, ALK1, and 5HTT mutations, other modifier genes are likely important in the pathogenesis of the disease. Thus, a multiple-hit theory seems to apply, similar to that often invoked for the development of cancers in which susceptible persons with a genetic predisposition require additional insults before manifesting the disease. Expanded natural history studies and further evaluation of persons at risk for pulmonary arterial hypertension (e.g., those with mutations of the TGF-β pathway and other identified mutations), as well as a better understanding of the disease-modifying genetic and acquired determinants, will provide improved insight into the relation between these genotypes and this complicated phenotype." @default.
- W216954906 created "2016-06-24" @default.
- W216954906 creator A5032869220 @default.
- W216954906 date "2008-05-04" @default.
- W216954906 modified "2023-09-26" @default.
- W216954906 title "Pathophysiology of Pulmonary Arterial Hypertension" @default.
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- W216954906 doi "https://doi.org/10.1007/978-1-60327-075-5_4" @default.
- W216954906 hasPublicationYear "2008" @default.
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