Key result
Abnormalities in endothelial function likely play a central role in mediating structural changes in pulmonary arterial hypertension, regardless of etiology.
Endothelial dysfunction is central to the structural changes and pathophysiology of pulmonary arterial hypertension.
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May inform endothelial-targeted therapy development in PAH; leaves open effects on progression across etiologies.
The mechanisms leading to elevations in precapillary pulmonary vascular resistance are complex and likely involve multiple pathways, but the histopathologic sequelae of these processes are restricted to a few findings, primarily neoangiogenesis, intimal and smooth muscle proliferation, vasoconstriction, and/or in situ thrombosis. Regardless of the etiology of pulmonary hypertension, abnormalities in endothelial function are often observed and likely play a central role in mediating structural changes.
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Jain et al. (2007) conducted a review in Pulmonary Arterial Hypertension. Abnormalities in endothelial function likely play a central role in mediating structural changes in pulmonary arterial hypertension, regardless of etiology.
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