ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Neutrophil-Endothelium Interaction Mediated by S100A9 Promotes Pulmonary Vascular Remodeling During Pulmonary Hypertension.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Article
- Recent advances in immunoregulatory biomaterials for tendon healing: From immune remodeling to functional regeneration.Materials today. Bio · 2026Review
- R213G-Mediated Redistribution of EC-SOD Protects Against Sugen-Hypoxia Pulmonary Hypertension in Mice.Pulmonary circulation · 2026Article
- The Role of Platelets in Pulmonary Hypertension: From Activation to Pulmonary Vascular Remodeling-A Review Article.Biomedicines · 2026Review
- Advances in the pathogenesis and clinical management of pulmonary hypertension.Medical review (2021) · 2026Review
- Pathophysiological mechanisms and therapeutic potential of E-selectin in pulmonary arterial hypertension.Frontiers in immunology · 2026Review
- The Endothelial Cell Perspective in Pulmonary Fibrosis: From Cell Fate Decisions, Intercellular Communication, and EndoMT to Emerging Therapies.Canadian respiratory journal · 2026Review
- Neutrophil-Endothelium Interaction Mediated by S100A9 Promotes Pulmonary Vascular Remodeling During Pulmonary Hypertension.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
14 authors.
Funding
Abstract
Pulmonary hypertension (PH) is a severe disease characterized by pulmonary vascular remodeling in which various immune cells play a critical role in vascular remodeling, although the details are still vague. Furthermore, current clinical treatments primarily focus on pulmonary vasodilation, but do not fundamentally address vascular remodeling itself. Here, first significant changes in neutrophils during the development of PH are demonstrated and show that neutrophil depletion can effectively attenuate disease progression. Moreover, the data show that neutrophil-derived S100A9 is the key mediator to promote vascular remodeling, while both knockout and inhibition of S100A9 can prevent PH. In a co-culture system of neutrophils and endothelial cells (ECs), hypoxic stimulation leads to increased S100A9 secretion by neutrophils, which activates the RAGE/PI3K/AKT pathway and causes dysfunction of ECs. These findings suggest that neutrophil-derived S100A9 mediated neutrophil-EC crosstalk plays an important role in pulmonary vascular remodeling, providing a promising strategy for treatment of PH.
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