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Is galectin-3 a biomarker, a player—or both—in the presence of coronary atherosclerosis?
Atherosclerosis is a complex process mediated by leukocytes, macrophages and various inflammatory markers. Galectin-3 is secreted by activated macrophages and is involved in cardiac fibrosis, cardiac remodeling, and inflammation. The present study aimed to determine the relationship between the pres...
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Published in: | Journal of investigative medicine 2016-03, Vol.64 (3), p.764-770 |
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creator | Aksan, Gökhan Gedikli, Ömer Keskin, Kudret Nar, Gökay İnci, Sinan Yıldız, Süleyman Sezai Kaplan, Özgür Soylu, Korhan Kılıçkesmez, Kadriye Orta Şahin, Mahmut |
description | Atherosclerosis is a complex process mediated by leukocytes, macrophages and various inflammatory markers. Galectin-3 is secreted by activated macrophages and is involved in cardiac fibrosis, cardiac remodeling, and inflammation. The present study aimed to determine the relationship between the presence and severity of coronary artery disease (CAD) and serum galectin-3 levels. The study included 82 patients with CAD confirmed via coronary angiography and 82 healthy participants as control group. Angiographic CAD was defined as ≥50% luminal diameter stenosis of at least one major epicardial coronary artery. The severity of CAD was determined by the Gensini score; and the serum galectin-3 levels were measured via ELISA. Serum galectin-3 levels were significantly higher in the patient group with CAD than in the control group (12.96±4.92 vs 5.52±1.9 ng/mL, p |
doi_str_mv | 10.1136/jim-2015-000041 |
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Galectin-3 is secreted by activated macrophages and is involved in cardiac fibrosis, cardiac remodeling, and inflammation. The present study aimed to determine the relationship between the presence and severity of coronary artery disease (CAD) and serum galectin-3 levels. The study included 82 patients with CAD confirmed via coronary angiography and 82 healthy participants as control group. Angiographic CAD was defined as ≥50% luminal diameter stenosis of at least one major epicardial coronary artery. The severity of CAD was determined by the Gensini score; and the serum galectin-3 levels were measured via ELISA. Serum galectin-3 levels were significantly higher in the patient group with CAD than in the control group (12.96±4.92 vs 5.52±1.9 ng/mL, p<0.001). In the correlation analysis, serum galectin-3 showed significant correlation with the Gensini score (r=0.715, p<0.001), number of diseased vessels (r=0.752, p<0.001) and serum hs-CRP level (r=0.607, p<0.001). In addition, multivariate logistic regression analysis showed that the serum galectin-3 levels were significant and independent predictors of the presence of angiographic CAD (OR=3.933, 95% CI 2.395 to 6.457; p<0.001). In the present study, the serum galectin-3 levels were higher in the patients with CAD than in healthy controls. Also, serum galectin-3 levels showed a significant positive correlation with the severity of CAD. An increased serum galectin-3 level may be considered an important activator and a marker of the atherosclerotic inflammatory process in CAD.</description><identifier>ISSN: 1081-5589</identifier><identifier>EISSN: 1708-8267</identifier><identifier>DOI: 10.1136/jim-2015-000041</identifier><identifier>PMID: 26912009</identifier><language>eng</language><publisher>Los Angeles, CA: SAGE Publications</publisher><subject>Atherosclerosis ; Atherosclerosis - blood ; Biomarkers ; Biomarkers - blood ; C-Reactive Protein - metabolism ; Cardiovascular disease ; Case-Control Studies ; Coronary Angiography ; Coronary Artery Disease - blood ; Female ; Galectin 3 - blood ; Humans ; Inflammation ; Logistic Models ; Male ; Middle Aged ; Proteins ; Risk Factors</subject><ispartof>Journal of investigative medicine, 2016-03, Vol.64 (3), p.764-770</ispartof><rights>Copyright © 2016 American Federation for Medical Research</rights><rights>2016 American Federation for Medical Research</rights><rights>Copyright © 2016 American Federation for Medical Research.</rights><rights>Copyright: 2016 Copyright (c) 2016 American Federation for Medical Research</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b397t-beee0c10b92d20658ac13348c9f41aa988594404f94204ecb5933a39fa1bea973</citedby><cites>FETCH-LOGICAL-b397t-beee0c10b92d20658ac13348c9f41aa988594404f94204ecb5933a39fa1bea973</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/1786935320/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$H</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1786935320?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,777,781,21357,21375,27905,27906,33592,33593,33750,33751,43714,43795,73970,74059</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26912009$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Aksan, Gökhan</creatorcontrib><creatorcontrib>Gedikli, Ömer</creatorcontrib><creatorcontrib>Keskin, Kudret</creatorcontrib><creatorcontrib>Nar, Gökay</creatorcontrib><creatorcontrib>İnci, Sinan</creatorcontrib><creatorcontrib>Yıldız, Süleyman Sezai</creatorcontrib><creatorcontrib>Kaplan, Özgür</creatorcontrib><creatorcontrib>Soylu, Korhan</creatorcontrib><creatorcontrib>Kılıçkesmez, Kadriye Orta</creatorcontrib><creatorcontrib>Şahin, Mahmut</creatorcontrib><title>Is galectin-3 a biomarker, a player—or both—in the presence of coronary atherosclerosis?</title><title>Journal of investigative medicine</title><addtitle>J Investig Med</addtitle><description>Atherosclerosis is a complex process mediated by leukocytes, macrophages and various inflammatory markers. Galectin-3 is secreted by activated macrophages and is involved in cardiac fibrosis, cardiac remodeling, and inflammation. The present study aimed to determine the relationship between the presence and severity of coronary artery disease (CAD) and serum galectin-3 levels. The study included 82 patients with CAD confirmed via coronary angiography and 82 healthy participants as control group. Angiographic CAD was defined as ≥50% luminal diameter stenosis of at least one major epicardial coronary artery. The severity of CAD was determined by the Gensini score; and the serum galectin-3 levels were measured via ELISA. Serum galectin-3 levels were significantly higher in the patient group with CAD than in the control group (12.96±4.92 vs 5.52±1.9 ng/mL, p<0.001). In the correlation analysis, serum galectin-3 showed significant correlation with the Gensini score (r=0.715, p<0.001), number of diseased vessels (r=0.752, p<0.001) and serum hs-CRP level (r=0.607, p<0.001). In addition, multivariate logistic regression analysis showed that the serum galectin-3 levels were significant and independent predictors of the presence of angiographic CAD (OR=3.933, 95% CI 2.395 to 6.457; p<0.001). In the present study, the serum galectin-3 levels were higher in the patients with CAD than in healthy controls. Also, serum galectin-3 levels showed a significant positive correlation with the severity of CAD. An increased serum galectin-3 level may be considered an important activator and a marker of the atherosclerotic inflammatory process in CAD.</description><subject>Atherosclerosis</subject><subject>Atherosclerosis - blood</subject><subject>Biomarkers</subject><subject>Biomarkers - blood</subject><subject>C-Reactive Protein - metabolism</subject><subject>Cardiovascular disease</subject><subject>Case-Control Studies</subject><subject>Coronary Angiography</subject><subject>Coronary Artery Disease - blood</subject><subject>Female</subject><subject>Galectin 3 - blood</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Logistic Models</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Proteins</subject><subject>Risk Factors</subject><issn>1081-5589</issn><issn>1708-8267</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>ALSLI</sourceid><sourceid>BGRYB</sourceid><sourceid>M0O</sourceid><recordid>eNqFkMtKxDAUhoMo3tfuJOBGxDq5NGmyEhm8geBGd0JJ4ql2bJsx6Sxm50P4hD6JGTqKCGIWyQn58p_kQ2iPkhNKuRxN6jZjhIqMpJHTFbRJC6IyxWSxmmqiaCaE0htoK8YJIUwKzdbRBpOaMkL0Jnq4jvjJNOD6uss4NtjWvjXhBcJx2kwbM4fw8fbuA7a-f05V3eH-GfA0QITOAfYVdj74zoQ5Nukk-OiaxVzH0x20Vpkmwu5y3Ub3F-d346vs5vbyenx2k1muiz6zAEAcJVazR0akUMZRznPldJVTY7RSQuc5ySudM5KDs0JzbriuDLVgdMG30eGQOw3-dQaxL9s6Omga04GfxZIWUglJi0Im9OAXOvGz0KXXJUpJzQVnJFGjgXLpIzFAVU5DnbTMS0rKhfgyiS8X4stBfLqxv8yd2RYev_kv0wk4HoBonuBH0z_zjgbctpN_m38CmFuZvQ</recordid><startdate>20160301</startdate><enddate>20160301</enddate><creator>Aksan, Gökhan</creator><creator>Gedikli, Ömer</creator><creator>Keskin, Kudret</creator><creator>Nar, Gökay</creator><creator>İnci, Sinan</creator><creator>Yıldız, Süleyman Sezai</creator><creator>Kaplan, Özgür</creator><creator>Soylu, Korhan</creator><creator>Kılıçkesmez, Kadriye Orta</creator><creator>Şahin, Mahmut</creator><general>SAGE Publications</general><general>Sage Publications Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>0-V</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AM</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ALSLI</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BGRYB</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K7.</scope><scope>K9.</scope><scope>M0O</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20160301</creationdate><title>Is galectin-3 a biomarker, a player—or both—in the presence of coronary atherosclerosis?</title><author>Aksan, Gökhan ; 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Galectin-3 is secreted by activated macrophages and is involved in cardiac fibrosis, cardiac remodeling, and inflammation. The present study aimed to determine the relationship between the presence and severity of coronary artery disease (CAD) and serum galectin-3 levels. The study included 82 patients with CAD confirmed via coronary angiography and 82 healthy participants as control group. Angiographic CAD was defined as ≥50% luminal diameter stenosis of at least one major epicardial coronary artery. The severity of CAD was determined by the Gensini score; and the serum galectin-3 levels were measured via ELISA. Serum galectin-3 levels were significantly higher in the patient group with CAD than in the control group (12.96±4.92 vs 5.52±1.9 ng/mL, p<0.001). In the correlation analysis, serum galectin-3 showed significant correlation with the Gensini score (r=0.715, p<0.001), number of diseased vessels (r=0.752, p<0.001) and serum hs-CRP level (r=0.607, p<0.001). In addition, multivariate logistic regression analysis showed that the serum galectin-3 levels were significant and independent predictors of the presence of angiographic CAD (OR=3.933, 95% CI 2.395 to 6.457; p<0.001). In the present study, the serum galectin-3 levels were higher in the patients with CAD than in healthy controls. Also, serum galectin-3 levels showed a significant positive correlation with the severity of CAD. An increased serum galectin-3 level may be considered an important activator and a marker of the atherosclerotic inflammatory process in CAD.</abstract><cop>Los Angeles, CA</cop><pub>SAGE Publications</pub><pmid>26912009</pmid><doi>10.1136/jim-2015-000041</doi><tpages>7</tpages></addata></record> |
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subjects | Atherosclerosis Atherosclerosis - blood Biomarkers Biomarkers - blood C-Reactive Protein - metabolism Cardiovascular disease Case-Control Studies Coronary Angiography Coronary Artery Disease - blood Female Galectin 3 - blood Humans Inflammation Logistic Models Male Middle Aged Proteins Risk Factors |
title | Is galectin-3 a biomarker, a player—or both—in the presence of coronary atherosclerosis? |
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