Abstract
Pulmonary arterial hypertension (PAH) is a progressive disease characterized by pulmonary vascular remodeling of the distal pulmonary vasculature, ultimately leading to destruction and loss of the smallest pulmonary arteries.1 The ensuing syndrome of PAH is clinically characterized by reduced pulmonary arterial circulatory flow, resulting in increased pulmonary vascular resistance, which ultimately results in failure of the right heart.2 In both children and adults, PAH presents as a primary disease or in association with a diverse range of diseases such as connective tissue diseases, portal hypertension, and congenital heart disease.3 Nearly all forms of World Health Organization (WHO) Group 1 PAH demonstrate a skewed gender ratio with significantly more females diagnosed with PAH than males.4–6 While the mechanistic details behind the female predominance remain unclear, this gender discrepancy may represent an opportunity for advanced biologic understanding and future therapeutic development. This article will briefly discuss the intersection of human, in vitro, and animal studies of PAH, and highlight the conflicting data that others have discussed and elegantly elaborated upon as the “estrogen paradox” in PAH.7–9
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