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Updated: Jul 15, 2026

Increasing Pulmonary Artery Pulsatile Flow Improves Hypoxic Pulmonary Hypertension in Piglets
Published on: May 11, 2015
Hypoxia-injured pulmonary vascular targeting and microenvironment-responsive nanoparticle to treat hypoxic pulmonary
Hongyan Wu1, Ruilin Zhou2, Wenting Hui1
1Department of Pharmaceutics, School of Pharmacy, Air Force Medical University, Xi'an, 710032, China.
Abstract:
Hypoxic pulmonary hypertension (HPH) is characterized by sustained pulmonary vasoconstriction and vascular remodeling caused by chronic hypoxia. The vicious cycle between hypoxia-inducible factor-1α (HIF-1α) activation and reactive oxygen species (ROS) burst release plays a central role in disease progression. P-selectin is overexpressed on hypoxia-injured pulmonary vascular endothelial cells and pulmonary smooth muscle cells. Fucoidan (Fuco) is a high-affinity ligand for P-selectin. Based on this, a hypoxia-injured pulmonary vascular targeting drug delivery system siHIF-1α/PSS31@Fuco (HPF) was developed. HPF was able to target for hypoxia-injured pulmonary vascular endothelial cells and pulmonary smooth muscle cells via the P-selectin, then HPF was taken up by those cells via caveolin-1-dependent endocytosis. Subsequently, the ROS-triggered depolymerization of PSS31 ensured efficient cytosolic release of siHIF-1α and SS31 to efficiently inhibit the expression of HIF-1α and the production of ROS, respectively. In HPH rats, HPF alleviated pulmonary vascular remodeling and improved the hemodynamics and right ventricular function by breaking the vicious cycle between HIF-1α activation and ROS production. Therefore, HPF is a promising nanotherapeutic strategy for HPH.
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