ArticleLung2025
FLRT3 Overexpression Attenuates Ischemia-Reperfusion Induced Vascular Hyperpermeability and Lung Injury Through RND3.
Article in Lung, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- Sex-Specific Pathophysiological Signatures in Allometric Dosing-Controlled Bleomycin Acute Lung Injury Model.bioRxiv : the preprint server for biology · 2026Article
- LncRNA RNF144A-AS1 increases P300-mediated H4K5 acetylation of PDE4 to promote keloid fibrosis.Biomedical engineering online · 2026Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
purposePulmonary ischemia/reperfusion injury (IRI) causes endothelial barrier dysfunction and increased vascular permeability. Fibronectin leucine-rich transmembrane protein-3 (FLRT3) is known to regulate endothelial cell function, but its role in pulmonary IRI remains unexplored.
methodsWe established both a mouse lung I/R model and a hypoxia/reoxygenation (H/R) cell culture model using human pulmonary microvascular endothelial cells (HPMECs). The effects of FLRT3 manipulation were assessed through lentiviral-mediated overexpression and knockdown approaches. Lung injury was evaluated by histological analysis, immunohistochemistry, and lung injury scoring. Endothelial barrier function was assessed using transmission electron microscopy, Evans blue extravasation, and endothelial permeability assays.
resultsFLRT3 expression was predominantly localized in pulmonary endothelial cells and was downregulated following I/R injury. Lentiviral vectors overexpressing FLRT3 (LV-FLRT3, 1 × 10
conclusionsOur findings reveal FLRT3, a critical regulator of endothelial barrier function during IRI through the RND3-RhoA pathway, is a potential therapeutic target for pulmonary IRI.
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Registered trials
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