ArticleMolecular medicine reports2017
Galectin-3 inhibition ameliorates hypoxia-induced pulmonary artery hypertension.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- Activation of PBK by Gal-3 contributes to pulmonary artery hypertension by promoting PRC1 activation.Respiratory research · 2026Article
- Glycopolymer Inhibitors of Galectin-3 Suppress the Markers of Tissue Remodeling in Pulmonary Hypertension.Journal of medicinal chemistry · 2024Article
- The Role of Galectin-3 in Heart Failure-The Diagnostic, Prognostic and Therapeutic Potential-Where Do We Stand?International journal of molecular sciences · 2023Review
- Smooth Muscle Cell Phenotypic Switch Induced by Traditional Cigarette Smoke Condensate: A Holistic Overview.International journal of molecular sciences · 2023Article
- A placenta-on-a-chip model to determine the regulation of FKBPL and galectin-3 in preeclampsia.Cellular and molecular life sciences : CMLS · 2023Article
- Prognostic value of galectin-3 and right ventricular function for long-term mortality in heart failure patients treated with cardiac resynchronization therapy.Scientific reports · 2021Article
- Activation of AMPK inhibits Galectin-3-induced pulmonary artery smooth muscle cells proliferation by upregulating hippo signaling effector YAP.Molecular and cellular biochemistry · 2021Article
- CRISPR/Cas9 Mediated Deletion of the Angiotensinogen Gene Reduces Hypertension: A Potential for Cure?Hypertension (Dallas, Tex. : 1979) · 2021Article
- Endothelial-to-Mesenchymal Transition in Pulmonary Arterial Hypertension.Antioxidants & redox signaling · 2021Review
- Galectin-3 Promotes ROS, Inflammation, and Vascular Fibrosis in Pulmonary Arterial Hypertension.Advances in experimental medicine and biology · 2021Article
- Galectin-3 is related to right ventricular dysfunction in heart failure patients with reduced ejection fraction and may affect exercise capacity.Scientific reports · 2020Article
- Hyperinflammation and Fibrosis in Severe COVID-19 Patients: Galectin-3, a Target Molecule to Consider.Frontiers in immunology · 2020Article
- Galectin-3: A Harbinger of Reactive Oxygen Species, Fibrosis, and Inflammation in Pulmonary Arterial Hypertension.Antioxidants & redox signaling · 2019Review
- Galectin-3 Mediates Endothelial-to-Mesenchymal Transition in Pulmonary Arterial Hypertension.Aging and disease · 2019Article
- Galectin-3 is expressed in vascular smooth muscle cells and promotes pulmonary hypertension through changes in proliferation, apoptosis, and fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Galectin-3 Promotes Vascular Remodeling and Contributes to Pulmonary Hypertension.American journal of respiratory and critical care medicine · 2018Article
- Article
- RNAi therapy to the wall of arteries and veins: anatomical, physiologic, and pharmacological considerations.Journal of translational medicine · 2017Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Galectin-3 (Gal-3) is a β-galactoside-binding lectin, which is important in inflammation, fibrosis and heart failure. The present study aimed to investigate the role and mechanism of Gal-3 in hypoxia-induced pulmonary arterial hypertension (PAH). Male C57BL/6J and Gal‑3‑/‑ mice were exposed to hypoxia, then the right ventricular systolic pressure (RVSP) and Fulton's index were measured, and Gal‑3 mRNA and protein expression in the pulmonary arteries was analyzed by reverse transcription‑quantitative polymerase chain reaction and western blotting. Compared with the control, hypoxia increased the mRNA and protein expression levels of Gal‑3 in wild type murine pulmonary arteries. Gal‑3 deletion reduced the hypoxia‑induced upregulation of RVSP and Fulton's index. Furthermore, human pulmonary arterial endothelial cells (HPAECs) and human pulmonary arterial smooth muscle cells (HPASMCs) were stimulated by hypoxia in vitro, and Gal‑3 expression was inhibited by small interfering RNA. The inflammatory response of HPAECs, and the proliferation and cell cycle distribution of HPASMCs was also analyzed. Gal‑3 inhibition alleviated the hypoxia‑induced inflammatory response in HPAECs, including tumor necrosis factor‑α and interleukin‑1 secretion, expression of intercellular adhesion molecule‑1 and adhesion of THP‑1 monocytes. Gal‑3 inhibition also reduced hypoxia‑induced proliferation of HPASMCs, partially by reducing cyclin D1 expression and increasing p27 expression. Furthermore, Gal‑3 inhibition suppressed HPASMC switching from a 'contractile' to a 'synthetic' phenotype. In conclusion, Gal‑3 serves a fundamental role in hypoxia‑induced PAH, and inhibition of Gal‑3 may represent a novel therapeutic target for the treatment of hypoxia-induced PAH.
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Registered trials
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