ArticleAging and disease2019
Galectin-3 Mediates Endothelial-to-Mesenchymal Transition in Pulmonary Arterial Hypertension.
Article in Aging and disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 43 citations in OpenAlex.
- From nanotechnology to immunomodulation: emerging strategies targeting macrophages in high altitude pulmonary hypertension.Journal of nanobiotechnology · 2026Review
- Endothelial MLKL Inhibition Reduces Hyperoxia-Induced Bronchopulmonary Dysplasia in Neonatal Mice.Journal of cellular and molecular medicine · 2026Article
- Pathology-tailored nanotherapy via Galectin-3-targeted and triple-responsive nanoparticles enables multimodal therapy against aortic dissection.Journal of nanobiotechnology · 2026Article
- Galectin-3 and the Glyco-Inflammatory Axis: A Missing Link to Residual Cardiovascular Risk in Coronary Artery Disease.Biomedicines · 2025Review
- Endothelial glycosylation and its emerging role in pulmonary vascular health and disease.Nature communications · 2025Review
- Endothelial-to-mesenchymal transition in the central nervous system: A potential therapeutic target to combat age-related vascular fragility.The Journal of pharmacology and experimental therapeutics · 2025Review
- Loss of Type 2 Bone Morphogenetic Protein Receptor Activates NOD-Like Receptor Family Protein 3/Gasdermin E-Mediated Pyroptosis in Pulmonary Arterial Hypertension.Journal of the American Heart Association · 2025Article
- Mechanisms Controlling the Behavior of Vascular Smooth Muscle Cells in Hypoxic Pulmonary Hypertension.Physiological research · 2024Review
- Knockdown of the long noncoding RNA VSIG2-1:1 promotes the angiogenic ability of human pulmonary microvascular endothelial cells by activating the VEGF/PI3K/AKT pathway.Respiratory research · 2024Article
- Review
- Glycopolymer Inhibitors of Galectin-3 Suppress the Markers of Tissue Remodeling in Pulmonary Hypertension.Journal of medicinal chemistry · 2024Article
- Sex-specific role of galectin-3 in aortic stenosis.Biology of sex differences · 2023Article
- Antibody-mediated neutralization of galectin-3 as a strategy for the treatment of systemic sclerosis.Nature communications · 2023Article
- Novel lncRNA LNC_000113 Drives the Activation of Pulmonary Adventitial Fibroblasts through Modulating PTEN/Akt/FoxO1 Pathway.Journal of cardiovascular development and disease · 2023Article
- Silencing TUFM Inhibits Development of Monocrotaline-Induced Pulmonary Hypertension by Regulating Mitochondrial Autophagy via AMPK/mTOR Signal Pathway.Oxidative medicine and cellular longevity · 2022Article
- The role of β-catenin in pulmonary artery endothelial-mesenchymal transformation in rats with chronic thromboembolic pulmonary hypertension.Journal of thrombosis and thrombolysis · 2021Article
- Article
- Genetic Delivery and Gene Therapy in Pulmonary Hypertension.International journal of molecular sciences · 2021Review
- Imaging atherosclerotic plaques by targeting Galectin-3 and activated macrophages using (Theranostics · 2021Article
- The hallmarks of severe pulmonary arterial hypertension: the cancer hypothesis-ten years later.American journal of physiology. Lung cellular and molecular physiology · 2020Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Galectin-3 (Gal-3) is highly expressed in fibrotic tissue related to diverse etiologies. endothelial-to-mesenchymal transition (EndoMT), A less well studied phenomenon serves as a critical process in pulmonary vascular remodeling associated with the development of pulmonary arterial hypertension (PAH). EndoMT is hypothesized to contribute to the over-proliferation of αSMA positive cells. We aim to investigate the potential role of Gal-3 in regulating EndoMT in PAH. We observed an upregulation in both Gal-3 and αSMA expression in the monocrotaline (MCT) and Hypoxia PAH model, accompanied with intimal thickening. For more profound vascular remodeling and endothelial layer lesion in former model, we employed Gal-3 knockdown and overexpression lentivirus methodology to the MCT rats to determine the mechanisms underlying abnormal endothelial cell transition in PAH. PAH was evaluated according to right ventricular systolic pressure, right heart hypertrophy and pulmonary artery remodeling. A reduction in Gal-3 was protective against the development of PAH, while Gal-3 upregulation aggravated pulmonary vascular occlusion. In addition, Gal-3 deficiency suppressed pulmonary vascular cell proliferation and macrophage infiltration. Finally, we revealed that in endothelial cells treated with tumor necrosis factor α and hypoxia (representing an
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