ArticleFrontiers in physiology2026
Transcriptomic profiling of the sex-linked biological pathways of severe pulmonary arterial hypertension associated with endothelial cell caveolin-1 depletion and chronic hypoxia.
Article in Frontiers in physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Pulmonary arterial hypertension (PAH) is distinguished by elevated blood pressure and vascular resistance in the arteries of the lungs. Patients with PAH demonstrate pulmonary vascular remodeling, wall thickening, and a high rate of morbidity due to right heart failure. Notably, while female patients are more likely to develop PAH, male patients suffer from higher morbidity rates after diagnosis. The molecular mechanism(s) underlying PAH development is poorly understood, though heritable PAH linked to mutations in bone morphogenic protein receptor 2 ( Methods: To interrogate this dynamic, we utilized a global Results: Both female and male Cav1 Discussion: These data indicate that muscle cell development, angiogenesis, cilia assembly, immune response, and BMP signaling pathways undergo sex-specific transcriptional regulation during PAH development that may underlie sex differences in PAH patient outcome.
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