ArticleMolecular medicine reports2017
Modified citrus pectin inhibits galectin-3 function to reduce atherosclerotic lesions in apoE-deficient mice.
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 24 papers.
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Who cites it
24 citing papers in PubMed, 43 citations in OpenAlex.
- Article
- Retinol-binding protein 4 in cardiovascular diseases: mechanisms and therapeutic perspectives.Frontiers in cardiovascular medicine · 2026Review
- The Role of Galectin-3 in Atherosclerosis and Its Cardiovascular Complications: An Update.Journal of lipid and atherosclerosis · 2026Review
- Pleiotropic regulatory mechanisms and targeted therapeutic prospects of Galectin-3 in aging-related diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Porcine milk small extracellular vesicles modulate peripheral blood mononuclear cell proteome in vitro.Scientific reports · 2025Article
- Citrus pectin-coated inhalable PLGA nanoparticles for treatment of pulmonary fibrosis.Journal of materials chemistry. B · 2025Article
- Galectin-3 in acute myocardial infarction: from molecular mechanisms to clinical translation.Frontiers in molecular biosciences · 2025Review
- Pectin: Health-promoting properties as a natural galectin-3 inhibitor.Glycoconjugate journal · 2024Review
- Galectin inhibitors and nanoparticles as a novel therapeutic strategy for glioblastoma multiforme.American journal of cancer research · 2024Review
- Galectin functions in cancer-associated inflammation and thrombosis.Frontiers in cardiovascular medicine · 2023Review
- Unraveling the role of galectin-3 in cardiac pathology and physiology.Frontiers in physiology · 2023Review
- The interplay of galectins-1, -3, and -9 in the immune-inflammatory response underlying cardiovascular and metabolic disease.Cardiovascular diabetology · 2022Review
- Early Doxorubicin Myocardial Injury: Inflammatory, Oxidative Stress, and Apoptotic Role of Galectin-3.International journal of molecular sciences · 2022Article
- The Diagnostic and Therapeutic Potential of Galectin-3 in Cardiovascular Diseases.Biomolecules · 2021Review
- Galectin-3 in Cardiovascular Diseases.International journal of molecular sciences · 2020Review
- New Classification of Macrophages in Plaques: a Revolution.Current atherosclerosis reports · 2020Review
- Pharmacological Inhibition of Galectin-3 Ameliorates Diabetes-Associated Cognitive Impairment, Oxidative Stress and Neuroinflammation in vivo and in vitro.Journal of inflammation research · 2020Article
- Galectin-3 Is a Potential Mediator for Atherosclerosis.Journal of immunology research · 2020Review
- Elevated Galectin-3 Plasma Concentrations in Recipients of Allogeneic Hematopoietic Cell Transplantation.Clinical hematology international · 2019Article
- Pleiotropic Effects of Modified Citrus Pectin.Nutrients · 2019Review
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Galectin-3 is a carbohydrate-binding lectin, which has been implicated in the modulation of atherosclerotic pathophysiology, and is highly expressed in monocytes, macrophages and endothelial cells within atherosclerotic plaques. Modified citrus pectin (MCP) is produced from citrus pectin via pH and temperature modifications, which break it into shorter, non‑branched, galactose‑rich carbohydrate chains. MCP is able to tightly bind with galectin‑3, via recognition of its carbohydrate recognition domain, and facilitates the modulation of galectin‑3‑induced bioactivity. The present study explored the effects of MCP on the initiation of atherosclerosis. Eight‑week‑old apolipoprotein E‑deficient mice were treated with 1% MCP and fed an atherogenic diet for 4 weeks. The effects of MCP on atherosclerotic initiation were determined by pathological analysis and scanning electron microscope (SEM) imaging. MCP treatment reduced the size of atherosclerotic lesion areas, which was accompanied by decreased numbers of macrophages and smooth muscle cells (SMCs). Furthermore, SEM examination of the surface of the atheroma‑prone vessel wall indicated that MCP treatment reduced endothelial injury. To analyze the effects of MCP on monocyte adhesion, firstly, oxidized‑low density lipoprotein and various concentrations of MCP (0.025, 0.05, 0.1 and 0.25%) were incubated with the human umbilical vein endothelial cells (HUVECs) for stimulation and following this, the U937 cells were plated onto the HUVECs. The results revealed that MCP reduced the adhesion of U937 monocytes to HUVECs, indicating the adhesion-inhibiting effects of MCP. In conclusion, the present study revealed that MCP, a galectin‑3 inhibitor, reduced the size of atherosclerotic lesions by inhibiting the adhesion of leucocytes to endothelial cells. Inhibition of galectin‑3 function may be a therapeutic strategy for the treatment of atherosclerosis.
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