Association between Omentin-1 and Coronary Artery Disease: Pathogenesis and Clinical Research

Like other adipokines, omentin-1 is secreted from visceral adipose tissue and plays a vital role in the development of chronic inflammatory diseases, including cardiovascular events. Recent studies have shown that circulating omentin-1 levels are associated with various metabolic risk factors, such...

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Autores principales: Askin, Lutfu, Duman, Hakan, Ozyıldız, Ali, Tanriverdi, Okan, Turkmen, Serdar
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Bentham Science Publishers 2020
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7536812/
https://www.ncbi.nlm.nih.gov/pubmed/32392116
http://dx.doi.org/10.2174/1573403X16666200511085304
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author Askin, Lutfu
Duman, Hakan
Ozyıldız, Ali
Tanriverdi, Okan
Turkmen, Serdar
author_facet Askin, Lutfu
Duman, Hakan
Ozyıldız, Ali
Tanriverdi, Okan
Turkmen, Serdar
author_sort Askin, Lutfu
collection PubMed
description Like other adipokines, omentin-1 is secreted from visceral adipose tissue and plays a vital role in the development of chronic inflammatory diseases, including cardiovascular events. Recent studies have shown that circulating omentin-1 levels are associated with various metabolic risk factors, such as high blood pressure, increased waist circumference, dyslipidemia, and glucose intolerance. The decrease in serum omentin level is an independent predictor of Coronary Artery Disease (CAD) and is associated with the severity of this disease. Since there is no relevant review in the literature, we aimed to summarize the studies on the relationship between omentin-1 and CAD.
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spelling pubmed-75368122021-08-01 Association between Omentin-1 and Coronary Artery Disease: Pathogenesis and Clinical Research Askin, Lutfu Duman, Hakan Ozyıldız, Ali Tanriverdi, Okan Turkmen, Serdar Curr Cardiol Rev Article Like other adipokines, omentin-1 is secreted from visceral adipose tissue and plays a vital role in the development of chronic inflammatory diseases, including cardiovascular events. Recent studies have shown that circulating omentin-1 levels are associated with various metabolic risk factors, such as high blood pressure, increased waist circumference, dyslipidemia, and glucose intolerance. The decrease in serum omentin level is an independent predictor of Coronary Artery Disease (CAD) and is associated with the severity of this disease. Since there is no relevant review in the literature, we aimed to summarize the studies on the relationship between omentin-1 and CAD. Bentham Science Publishers 2020-08 2020-08 /pmc/articles/PMC7536812/ /pubmed/32392116 http://dx.doi.org/10.2174/1573403X16666200511085304 Text en © 2020 Bentham Science Publishers https://creativecommons.org/licenses/by-nc/4.0/legalcode This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) (https://creativecommons.org/licenses/by-nc/4.0/legalcode), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.
spellingShingle Article
Askin, Lutfu
Duman, Hakan
Ozyıldız, Ali
Tanriverdi, Okan
Turkmen, Serdar
Association between Omentin-1 and Coronary Artery Disease: Pathogenesis and Clinical Research
title Association between Omentin-1 and Coronary Artery Disease: Pathogenesis and Clinical Research
title_full Association between Omentin-1 and Coronary Artery Disease: Pathogenesis and Clinical Research
title_fullStr Association between Omentin-1 and Coronary Artery Disease: Pathogenesis and Clinical Research
title_full_unstemmed Association between Omentin-1 and Coronary Artery Disease: Pathogenesis and Clinical Research
title_short Association between Omentin-1 and Coronary Artery Disease: Pathogenesis and Clinical Research
title_sort association between omentin-1 and coronary artery disease: pathogenesis and clinical research
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7536812/
https://www.ncbi.nlm.nih.gov/pubmed/32392116
http://dx.doi.org/10.2174/1573403X16666200511085304
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