Hypoxia-injured pulmonary vascular targeting and microenvironment-responsive nanoparticle to treat hypoxic pulmonary hypertension.

Authors

Hongyan Wu, Ruilin Zhou, Wenting Hui, Sai Qiao, Luoqi Zhang, Qifeng Ji, Miao Liu, Bangle Zhang, Shaobo Bai, Daozhou Liu, Siyuan Zhou

Published in

Journal of nanobiotechnology. Jul 13, 2026. Epub Jul 13, 2026.

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.

PMID:
42443954
Bibliographic data and abstract were imported from PubMed on 14 Jul 2026.

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