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Galectin-3 Is a Potential Mediator for Atherosclerosis
Atherosclerosis is a multifactorial chronic inflammatory arterial disease forming the pathological basis of many cardiovascular diseases such as coronary heart disease, heart failure, and stroke. Numerous studies have implicated inflammation as a key player in the initiation and progression of ather...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7042544/ https://www.ncbi.nlm.nih.gov/pubmed/32149158 http://dx.doi.org/10.1155/2020/5284728 |
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author | Gao, Ziyu Liu, Zhongni Wang, Rui Zheng, Yinghong Li, Hong Yang, Liming |
author_facet | Gao, Ziyu Liu, Zhongni Wang, Rui Zheng, Yinghong Li, Hong Yang, Liming |
author_sort | Gao, Ziyu |
collection | PubMed |
description | Atherosclerosis is a multifactorial chronic inflammatory arterial disease forming the pathological basis of many cardiovascular diseases such as coronary heart disease, heart failure, and stroke. Numerous studies have implicated inflammation as a key player in the initiation and progression of atherosclerosis. Galectin-3 (Gal-3) is a 30 kDa β-galactose, highly conserved and widely distributed intracellularly and extracellularly. Gal-3 has been demonstrated in recent years to be a novel inflammatory factor participating in the process of intravascular inflammation, lipid endocytosis, macrophage activation, cellular proliferation, monocyte chemotaxis, and cell adhesion. This review focuses on the role of Gal-3 in atherosclerosis and the mechanism involved and several classical Gal-3 agonists and antagonists in the current studies. |
format | Online Article Text |
id | pubmed-7042544 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-70425442020-03-07 Galectin-3 Is a Potential Mediator for Atherosclerosis Gao, Ziyu Liu, Zhongni Wang, Rui Zheng, Yinghong Li, Hong Yang, Liming J Immunol Res Review Article Atherosclerosis is a multifactorial chronic inflammatory arterial disease forming the pathological basis of many cardiovascular diseases such as coronary heart disease, heart failure, and stroke. Numerous studies have implicated inflammation as a key player in the initiation and progression of atherosclerosis. Galectin-3 (Gal-3) is a 30 kDa β-galactose, highly conserved and widely distributed intracellularly and extracellularly. Gal-3 has been demonstrated in recent years to be a novel inflammatory factor participating in the process of intravascular inflammation, lipid endocytosis, macrophage activation, cellular proliferation, monocyte chemotaxis, and cell adhesion. This review focuses on the role of Gal-3 in atherosclerosis and the mechanism involved and several classical Gal-3 agonists and antagonists in the current studies. Hindawi 2020-02-14 /pmc/articles/PMC7042544/ /pubmed/32149158 http://dx.doi.org/10.1155/2020/5284728 Text en Copyright © 2020 Ziyu Gao et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Gao, Ziyu Liu, Zhongni Wang, Rui Zheng, Yinghong Li, Hong Yang, Liming Galectin-3 Is a Potential Mediator for Atherosclerosis |
title | Galectin-3 Is a Potential Mediator for Atherosclerosis |
title_full | Galectin-3 Is a Potential Mediator for Atherosclerosis |
title_fullStr | Galectin-3 Is a Potential Mediator for Atherosclerosis |
title_full_unstemmed | Galectin-3 Is a Potential Mediator for Atherosclerosis |
title_short | Galectin-3 Is a Potential Mediator for Atherosclerosis |
title_sort | galectin-3 is a potential mediator for atherosclerosis |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7042544/ https://www.ncbi.nlm.nih.gov/pubmed/32149158 http://dx.doi.org/10.1155/2020/5284728 |
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