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Pulmonary endothelial cells (PECs) are specialized cells that form the inner lining of the pulmonary vasculature, serving as a critical interface between the blood and the lung tissue. They play a fundamental role in maintaining the blood-gas barrier, which is essential for efficient gas exchange while preventing the leakage of fluid into the alveoli (Stevens, 2011, American Journal of Physiology). Beyond their structural role, PECs are metabolically active, regulating vascular tone through the production of mediators like nitric oxide and endothelin-1, and managing immune cell trafficking during inflammation (Aird, 2007, Circulation Research). Dysfunction of the pulmonary endothelium is a central feature in the pathogenesis of diseases such as pulmonary arterial hypertension (PAH) and acute respiratory distress syndrome (ARDS) (Teuwen et al., 2019, Nature Reviews Cardiology). While PECs are a cell type rather than a single molecular target, they express various receptors and enzymes that are the focus of pharmacological interventions aimed at treating pulmonary vascular disorders (Huertas et al., 2018, European Respiratory Journal).
Pharmacological agents interact with pulmonary endothelial cells by modulating specific molecular pathways, such as the nitric oxide-cGMP pathway via PDE5 inhibition, the endothelin system via receptor antagonism, and the prostacyclin pathway through receptor agonism, to regulate vascular resistance and barrier integrity (StatPearls, 2023; NIH, 2022).
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