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- W2159448723 abstract "The striking female predominance in idiopathic and familial pulmonary arterial hypertension (PAH) has been well documented since the publication of the National Institutes of Health (NIH) registry in 1987 [1]. In the majority of PAH registries, females are at least twice as likely to be represented as males, with female to male ratios as high as four to one [2–6]. Notably, these sex differences are not fully explained by a differential distribution of known risk factors for PAH by sex, such as autoimmune disease or anorexigen exposure. Taken together, these epidemiological data suggest that other sex-associated factors, including sex hormones, may influence PAH pathogenesis.Endogenous and exogenous sex hormone exposures represent a biologically plausible potential risk factor for PAH. Sex hormones determine in utero organ development, drive tissue-specific changes in early life and exert an evolving influence across the life span as their absolute and relative concentrations shift [7]. There can be no doubt that sex hormones, with their ability to modulate vascular tone, inflammation and remodelling, play a fundamental role in determining cardiovascular phenotypes [8]. Emerging data on the importance of sex hormones in animal models of pulmonary hypertension provide tantalising evidence that the pulmonary vascular phenotype of an organism is dependent upon these pleiotropic signalling molecules [9, 10].In this issue of the European Respiratory Journal , Yuan et al. [11] demonstrate that monocrotaline (MCT) creates an oestrogen-deficient state in rats characterised by low plasma oestradiol (E2) and altered pulmonary expression of oestrogen receptors and enzymes responsible for E2 anabolism (reduced) and catabolism (increased). In the absence of sufficient endogenous ( i.e. post-ovariectomy) or exogenous oestradiol, a pro-proliferative, anti-apoptotic and vasoconstrictive phenotype emerges that is mediated in part via reduced nitric oxide and prostacyclin, and increased endothelin. Rescue of the …" @default.
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- W2159448723 date "2013-04-30" @default.
- W2159448723 modified "2023-09-25" @default.
- W2159448723 title "Oestrogen and the sexual dimorphism of pulmonary arterial hypertension: a translational challenge" @default.
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- W2159448723 doi "https://doi.org/10.1183/09031936.00021713" @default.
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