ArticleAdvances in experimental medicine and biology2021
Galectin-3 Promotes ROS, Inflammation, and Vascular Fibrosis in Pulmonary Arterial Hypertension.
Article in Advances in experimental medicine and biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Evidence for PDZ-Binding Kinase in Lung Disease With an Emphasis on PAH.Pulmonary circulation · 2026Review
- Expression, Localization and Actions of Galectin-3: Implications in the Pathophysiology and Therapy of Cardiovascular Disease.International journal of molecular sciences · 2026Review
- Activation of PBK by Gal-3 contributes to pulmonary artery hypertension by promoting PRC1 activation.Respiratory research · 2026Article
- Unraveling Non-coding RNAs and dysregulation of TGF-β signalling in cardiorenal syndrome, a focused review for molecular and clinical applications.Molecular biology reports · 2025Review
- Brain-Targeted Reactive Oxygen Species in Hypertension: Unveiling Subcellular Dynamics, Immune Cross-Talk, and Novel Therapeutic Pathways.Antioxidants (Basel, Switzerland) · 2025Review
- Can mac-2 binding protein glycosylation isomer serve as a biomarker for predicting pulmonary arterial pressure and pulmonary hypertension in systemic sclerosis?Turkish journal of medical sciences · 2025Article
- Review
- Galectin-3 and Severity of Liver Fibrosis in Metabolic Dysfunction-Associated Fatty Liver Disease.Protein and peptide letters · 2024Review
- Inhibition of LPS-Induced Inflammatory Response of Oral Mesenchymal Stem Cells in the Presence of Galectin-3.Biomedicines · 2023Article
- An emerging view on vascular fibrosis molecular mediators and relevant disorders: from bench to bed.Frontiers in cardiovascular medicine · 2023Review
- Heterozygous Loss of KRIT1 in Mice Affects Metabolic Functions of the Liver, Promoting Hepatic Oxidative and Glycative Stress.International journal of molecular sciences · 2022Article
- N-Acetylcysteine, an ROS Inhibitor, Alleviates the Pathophysiology of Hyperthyroidism-Induced Cardiomyopathy via the ROS/CaBiomolecules · 2022Article
- Mechanisms of pulmonary vascular dysfunction in pulmonary hypertension and implications for novel therapies.American journal of physiology. Heart and circulatory physiology · 2022Review
- Effects of the peripheral CBFrontiers in pharmacology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary Arterial Hypertension (PAH) is a progressive vascular disease arising from the narrowing of pulmonary arteries (PA) resulting in high pulmonary arterial blood pressure and ultimately right ventricular (RV) failure. A defining characteristic of PAH is the excessive remodeling of PA that includes increased proliferation, inflammation, and fibrosis. There is no cure for PAH nor interventions that effectively impede or reverse PA remodeling, and research over the past several decades has sought to identify novel molecular mechanisms of therapeutic benefit. Galectin-3 (Gal-3; Mac-2) is a carbohydrate-binding lectin that is remarkable for its chimeric structure, comprised of an N-terminal oligomerization domain and a C-terminal carbohydrate-recognition domain. Gal-3 is a regulator of changes in cell behavior that contribute to aberrant PA remodeling including cell proliferation, inflammation, and fibrosis, but its role in PAH is poorly understood. Herein, we summarize the recent literature on the role of Gal-3 in the development of PAH and provide experimental evidence supporting the ability of Gal-3 to influence reactive oxygen species (ROS) production, NOX enzyme expression, inflammation, and fibrosis, which contributes to PA remodeling. Finally, we address the clinical significance of Gal-3 as a target in the development of therapeutic agents as a treatment for PAH.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.