ArticleAmerican journal of physiology. Lung cellular and molecular physiology2019
Galectin-3 is expressed in vascular smooth muscle cells and promotes pulmonary hypertension through changes in proliferation, apoptosis, and fibrosis.
Article in American journal of physiology. Lung cellular and molecular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 81 citations in OpenAlex.
- Evidence for PDZ-Binding Kinase in Lung Disease With an Emphasis on PAH.Pulmonary circulation · 2026Review
- Macrophage-derived galectin-3 contributes to pyroptosis, apoptosis and necroptosis through TLR4/MyD88/NF-κB/NLRP3 during atherosclerosis.Clinical and translational medicine · 2026Article
- Activation of PBK by Gal-3 contributes to pulmonary artery hypertension by promoting PRC1 activation.Respiratory research · 2026Article
- Galectin-3 is dispensable for thoracic aortic aneurysmal formation and rupture in mice.JVS-vascular science · 2026Article
- Maternal Electronic Cigarette Exposure Induces Dysregulation of Autophagy via Oxidative Stress/DNA Methylation in Pulmonary Hypertension Offspring.Current medical science · 2025Article
- Sodium nitroprusside improves circulatory failure in rabbit acute pulmonary embolism combined with shock model possibly by enhancing NO release and inhibiting TLR4/NF-кB/HIF-1α signaling pathway.Frontiers in physiology · 2025Article
- Article
- Mechanisms Controlling the Behavior of Vascular Smooth Muscle Cells in Hypoxic Pulmonary Hypertension.Physiological research · 2024Review
- Review
- PDZ-Binding Kinase, a Novel Regulator of Vascular Remodeling in Pulmonary Arterial Hypertension.Circulation · 2024Article
- Ginsenoside Rg1 alleviates vascular remodeling in hypoxia-induced pulmonary hypertension mice through the calpain-1/STAT3 signaling pathway.Journal of ginseng research · 2024Article
- Novel Tryptophan Hydroxylase Inhibitor TPT-001 Reverses PAH, Vascular Remodeling, and Proliferative-Proinflammatory Gene Expression.JACC. Basic to translational science · 2024Article
- Glycopolymer Inhibitors of Galectin-3 Suppress the Markers of Tissue Remodeling in Pulmonary Hypertension.Journal of medicinal chemistry · 2024Article
- Galectin-3 Mediates Vascular Dysfunction in Obesity by Regulating NADPH Oxidase 1.Arteriosclerosis, thrombosis, and vascular biology · 2023Article
- [Quercetin improves pulmonary arterial hypertension in rats by regulating the HMGB1/RAGE/NF-κB pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 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
- Alleviating experimental pulmonary hypertensionActa pharmaceutica Sinica. B · 2023Article
- Silencing of NOTCH3 Signaling in Meniscus Smooth Muscle Cells Inhibits Fibrosis and Exacerbates Degeneration in a HEYL-Dependent Manner.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Positive Association of Serum Galectin-3 with the Development of Aortic Stiffness of Patients on Peritoneal Dialysis.Journal of clinical medicine · 2023Article
- Hpgd affects the progression of hypoxic pulmonary hypertension by regulating vascular remodeling.BMC pulmonary medicine · 2023Article
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Authors and funding
20 authors at 3 institutions in 3 countries.
Funding
Abstract
A defining characteristic of pulmonary hypertension (PH) is the extensive remodeling of pulmonary arteries (PAs), which results in progressive increases in vascular resistance and stiffness and eventual failure of the right ventricle. There is no cure for PH and identification of novel molecular mechanisms that underlie increased proliferation, reduced apoptosis, and excessive extracellular matrix production in pulmonary artery smooth muscle cells (PASMCs) is a vital objective. Galectin-3 (Gal-3) is a chimeric lectin and potent driver of many aspects of fibrosis, but its role in regulating PASMC behavior in PH remains poorly understood. Herein, we evaluated the importance of increased Gal-3 expression and signaling on PA vascular remodeling and cardiopulmonary function in experimental models of PH. Gal-3 expression was quantified by qRT-PCR, immunoblotting, and immunofluorescence imaging, and its functional role was assessed by specific Gal-3 inhibitors and CRISPR/Cas9-mediated knockout of Gal-3 in the rat. In rat models of PH, we observed increased Gal-3 expression in PASMCs, which stimulated migration and resistance to apoptosis, whereas silencing or genetic deletion reduced cellular migration and PA fibrosis and increased apoptosis. Gal-3 inhibitors attenuated and reversed PA remodeling and fibrosis, as well as hemodynamic indices in monocrotaline (MCT)-treated rats in vivo. These results were supported by genetic deletion of Gal-3 in both MCT and Sugen Hypoxia rat models. In conclusion, our results suggest that elevated Gal-3 levels contribute to inappropriate PA remodeling in PH by enhancing multiple profibrotic mechanisms. Therapeutic strategies targeting Gal-3 may be of benefit in the treatment of PH.
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