Role of galectin‐3 in subclinical myocardial impairment in psoriasis
Background Psoriasis has been shown to increase cardiovascular risk, and a contributor to this might be enhanced myocardial fibrosis promoted by the disease‐associated pro‐inflammatory milieu. Objective We sought to investigate the relationship of galectin‐3 (Gal‐3) – a recognized mediator of fibros...
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Published in | Journal of the European Academy of Dermatology and Venereology Vol. 33; no. 1; pp. 136 - 142 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
01.01.2019
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Subjects | |
Online Access | Get full text |
ISSN | 0926-9959 1468-3083 1468-3083 |
DOI | 10.1111/jdv.15211 |
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Abstract | Background
Psoriasis has been shown to increase cardiovascular risk, and a contributor to this might be enhanced myocardial fibrosis promoted by the disease‐associated pro‐inflammatory milieu.
Objective
We sought to investigate the relationship of galectin‐3 (Gal‐3) – a recognized mediator of fibrosis with inflammatory activation and left ventricular (LV) systolic and diastolic function in patients with psoriasis.
Methods
We enrolled 102 psoriatic patients (mean age: 52.5 ± 12.6 years). Sixty‐five age‐ and sex‐matched healthy subjects served as controls. Echocardiographic assessment of myocardial function included estimation of LV longitudinal systolic deformation (GLS) and diastolic indices: tissue e′ velocity and E/e′ ratio. Laboratory measurements encompassed blood Gal‐3, creatinine, glucose, insulin, CRP and erythrocyte sedimentation rate (ESR).
Results
Patients with psoriasis were characterized by elevated Gal‐3 (12.3 [9.3–13.4] vs. 6.3 [5.5–9.4] ng/mL in healthy controls, P < 0.001), ESR (17.0 [11.0–29.0] vs. 8.5 [6.0–13.0] mm, respectively, P < 0.001) and CRP (3.1 [1.7–10.6] vs. 1.9 [1.5–4.0] mg/L, respectively, P < 0.001), and reduced GLS (19.9 ± 3.7 vs. 22.0 ± 3.0%, respectively, P < 0.001). Progressive deterioration of GLS was demonstrated across Gal‐3 tertiles. Significant associations between GLS and age (beta = −0.21, P < 0.04), Gal‐3 (beta = −0.27, P < 0.01), CRP (beta = −0.22, P < 0.03), ESR (beta = −0.25, P < 0.01), waist circumference (beta = −0.22, P < 0.03) and waist‐to‐hip ratio (beta = −0.20, P < 0.05) were found. Stepwise multiple regression analysis revealed that the independent determinants of GLS in psoriatic patients were Gal‐3 (beta = −0.24, P < 0.01) and ESR (beta = −0.21, P < 0.03). Regression‐based mediation analysis demonstrated that the relationship between ESR and GLS was partially mediated by Gal‐3.
Conclusions
Subclinical left ventricular systolic dysfunction in psoriasis, as evidenced by reduced GLS, is linked with the inflammatory upregulation, and enhanced profibrotic activity (as reflected by elevated serum Gal‐3) may be involved in this process. These putative mechanisms may be responsible for the observed higher incidence of heart failure in this disease condition and should be considered as a potential target for preventive and therapeutic measures. |
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AbstractList | Psoriasis has been shown to increase cardiovascular risk, and a contributor to this might be enhanced myocardial fibrosis promoted by the disease-associated pro-inflammatory milieu.BACKGROUNDPsoriasis has been shown to increase cardiovascular risk, and a contributor to this might be enhanced myocardial fibrosis promoted by the disease-associated pro-inflammatory milieu.We sought to investigate the relationship of galectin-3 (Gal-3) - a recognized mediator of fibrosis with inflammatory activation and left ventricular (LV) systolic and diastolic function in patients with psoriasis.OBJECTIVEWe sought to investigate the relationship of galectin-3 (Gal-3) - a recognized mediator of fibrosis with inflammatory activation and left ventricular (LV) systolic and diastolic function in patients with psoriasis.We enrolled 102 psoriatic patients (mean age: 52.5 ± 12.6 years). Sixty-five age- and sex-matched healthy subjects served as controls. Echocardiographic assessment of myocardial function included estimation of LV longitudinal systolic deformation (GLS) and diastolic indices: tissue e' velocity and E/e' ratio. Laboratory measurements encompassed blood Gal-3, creatinine, glucose, insulin, CRP and erythrocyte sedimentation rate (ESR).METHODSWe enrolled 102 psoriatic patients (mean age: 52.5 ± 12.6 years). Sixty-five age- and sex-matched healthy subjects served as controls. Echocardiographic assessment of myocardial function included estimation of LV longitudinal systolic deformation (GLS) and diastolic indices: tissue e' velocity and E/e' ratio. Laboratory measurements encompassed blood Gal-3, creatinine, glucose, insulin, CRP and erythrocyte sedimentation rate (ESR).Patients with psoriasis were characterized by elevated Gal-3 (12.3 [9.3-13.4] vs. 6.3 [5.5-9.4] ng/mL in healthy controls, P < 0.001), ESR (17.0 [11.0-29.0] vs. 8.5 [6.0-13.0] mm, respectively, P < 0.001) and CRP (3.1 [1.7-10.6] vs. 1.9 [1.5-4.0] mg/L, respectively, P < 0.001), and reduced GLS (19.9 ± 3.7 vs. 22.0 ± 3.0%, respectively, P < 0.001). Progressive deterioration of GLS was demonstrated across Gal-3 tertiles. Significant associations between GLS and age (beta = -0.21, P < 0.04), Gal-3 (beta = -0.27, P < 0.01), CRP (beta = -0.22, P < 0.03), ESR (beta = -0.25, P < 0.01), waist circumference (beta = -0.22, P < 0.03) and waist-to-hip ratio (beta = -0.20, P < 0.05) were found. Stepwise multiple regression analysis revealed that the independent determinants of GLS in psoriatic patients were Gal-3 (beta = -0.24, P < 0.01) and ESR (beta = -0.21, P < 0.03). Regression-based mediation analysis demonstrated that the relationship between ESR and GLS was partially mediated by Gal-3.RESULTSPatients with psoriasis were characterized by elevated Gal-3 (12.3 [9.3-13.4] vs. 6.3 [5.5-9.4] ng/mL in healthy controls, P < 0.001), ESR (17.0 [11.0-29.0] vs. 8.5 [6.0-13.0] mm, respectively, P < 0.001) and CRP (3.1 [1.7-10.6] vs. 1.9 [1.5-4.0] mg/L, respectively, P < 0.001), and reduced GLS (19.9 ± 3.7 vs. 22.0 ± 3.0%, respectively, P < 0.001). Progressive deterioration of GLS was demonstrated across Gal-3 tertiles. Significant associations between GLS and age (beta = -0.21, P < 0.04), Gal-3 (beta = -0.27, P < 0.01), CRP (beta = -0.22, P < 0.03), ESR (beta = -0.25, P < 0.01), waist circumference (beta = -0.22, P < 0.03) and waist-to-hip ratio (beta = -0.20, P < 0.05) were found. Stepwise multiple regression analysis revealed that the independent determinants of GLS in psoriatic patients were Gal-3 (beta = -0.24, P < 0.01) and ESR (beta = -0.21, P < 0.03). Regression-based mediation analysis demonstrated that the relationship between ESR and GLS was partially mediated by Gal-3.Subclinical left ventricular systolic dysfunction in psoriasis, as evidenced by reduced GLS, is linked with the inflammatory upregulation, and enhanced profibrotic activity (as reflected by elevated serum Gal-3) may be involved in this process. These putative mechanisms may be responsible for the observed higher incidence of heart failure in this disease condition and should be considered as a potential target for preventive and therapeutic measures.CONCLUSIONSSubclinical left ventricular systolic dysfunction in psoriasis, as evidenced by reduced GLS, is linked with the inflammatory upregulation, and enhanced profibrotic activity (as reflected by elevated serum Gal-3) may be involved in this process. These putative mechanisms may be responsible for the observed higher incidence of heart failure in this disease condition and should be considered as a potential target for preventive and therapeutic measures. Psoriasis has been shown to increase cardiovascular risk, and a contributor to this might be enhanced myocardial fibrosis promoted by the disease-associated pro-inflammatory milieu. We sought to investigate the relationship of galectin-3 (Gal-3) - a recognized mediator of fibrosis with inflammatory activation and left ventricular (LV) systolic and diastolic function in patients with psoriasis. We enrolled 102 psoriatic patients (mean age: 52.5 ± 12.6 years). Sixty-five age- and sex-matched healthy subjects served as controls. Echocardiographic assessment of myocardial function included estimation of LV longitudinal systolic deformation (GLS) and diastolic indices: tissue e' velocity and E/e' ratio. Laboratory measurements encompassed blood Gal-3, creatinine, glucose, insulin, CRP and erythrocyte sedimentation rate (ESR). Patients with psoriasis were characterized by elevated Gal-3 (12.3 [9.3-13.4] vs. 6.3 [5.5-9.4] ng/mL in healthy controls, P < 0.001), ESR (17.0 [11.0-29.0] vs. 8.5 [6.0-13.0] mm, respectively, P < 0.001) and CRP (3.1 [1.7-10.6] vs. 1.9 [1.5-4.0] mg/L, respectively, P < 0.001), and reduced GLS (19.9 ± 3.7 vs. 22.0 ± 3.0%, respectively, P < 0.001). Progressive deterioration of GLS was demonstrated across Gal-3 tertiles. Significant associations between GLS and age (beta = -0.21, P < 0.04), Gal-3 (beta = -0.27, P < 0.01), CRP (beta = -0.22, P < 0.03), ESR (beta = -0.25, P < 0.01), waist circumference (beta = -0.22, P < 0.03) and waist-to-hip ratio (beta = -0.20, P < 0.05) were found. Stepwise multiple regression analysis revealed that the independent determinants of GLS in psoriatic patients were Gal-3 (beta = -0.24, P < 0.01) and ESR (beta = -0.21, P < 0.03). Regression-based mediation analysis demonstrated that the relationship between ESR and GLS was partially mediated by Gal-3. Subclinical left ventricular systolic dysfunction in psoriasis, as evidenced by reduced GLS, is linked with the inflammatory upregulation, and enhanced profibrotic activity (as reflected by elevated serum Gal-3) may be involved in this process. These putative mechanisms may be responsible for the observed higher incidence of heart failure in this disease condition and should be considered as a potential target for preventive and therapeutic measures. Background Psoriasis has been shown to increase cardiovascular risk, and a contributor to this might be enhanced myocardial fibrosis promoted by the disease‐associated pro‐inflammatory milieu. Objective We sought to investigate the relationship of galectin‐3 (Gal‐3) – a recognized mediator of fibrosis with inflammatory activation and left ventricular (LV) systolic and diastolic function in patients with psoriasis. Methods We enrolled 102 psoriatic patients (mean age: 52.5 ± 12.6 years). Sixty‐five age‐ and sex‐matched healthy subjects served as controls. Echocardiographic assessment of myocardial function included estimation of LV longitudinal systolic deformation (GLS) and diastolic indices: tissue e′ velocity and E/e′ ratio. Laboratory measurements encompassed blood Gal‐3, creatinine, glucose, insulin, CRP and erythrocyte sedimentation rate (ESR). Results Patients with psoriasis were characterized by elevated Gal‐3 (12.3 [9.3–13.4] vs. 6.3 [5.5–9.4] ng/mL in healthy controls, P < 0.001), ESR (17.0 [11.0–29.0] vs. 8.5 [6.0–13.0] mm, respectively, P < 0.001) and CRP (3.1 [1.7–10.6] vs. 1.9 [1.5–4.0] mg/L, respectively, P < 0.001), and reduced GLS (19.9 ± 3.7 vs. 22.0 ± 3.0%, respectively, P < 0.001). Progressive deterioration of GLS was demonstrated across Gal‐3 tertiles. Significant associations between GLS and age (beta = −0.21, P < 0.04), Gal‐3 (beta = −0.27, P < 0.01), CRP (beta = −0.22, P < 0.03), ESR (beta = −0.25, P < 0.01), waist circumference (beta = −0.22, P < 0.03) and waist‐to‐hip ratio (beta = −0.20, P < 0.05) were found. Stepwise multiple regression analysis revealed that the independent determinants of GLS in psoriatic patients were Gal‐3 (beta = −0.24, P < 0.01) and ESR (beta = −0.21, P < 0.03). Regression‐based mediation analysis demonstrated that the relationship between ESR and GLS was partially mediated by Gal‐3. Conclusions Subclinical left ventricular systolic dysfunction in psoriasis, as evidenced by reduced GLS, is linked with the inflammatory upregulation, and enhanced profibrotic activity (as reflected by elevated serum Gal‐3) may be involved in this process. These putative mechanisms may be responsible for the observed higher incidence of heart failure in this disease condition and should be considered as a potential target for preventive and therapeutic measures. |
Author | Rojek, A. Szepietowski, J.C. Karolko, B. Przewlocka‐Kosmala, M. Bednarek‐Tupikowska, G. Kosmala, W. Kabaj, M. Tupikowska‐Marzec, M. Kotwica, T. Maj, J. Relewicz, J. |
Author_xml | – sequence: 1 givenname: T. surname: Kotwica fullname: Kotwica, T. organization: Wroclaw Medical University – sequence: 2 givenname: J. surname: Relewicz fullname: Relewicz, J. organization: Wroclaw Medical University – sequence: 3 givenname: A. surname: Rojek fullname: Rojek, A. organization: Wroclaw Medical University – sequence: 4 givenname: M. surname: Tupikowska‐Marzec fullname: Tupikowska‐Marzec, M. organization: Wroclaw Medical University – sequence: 5 givenname: M. surname: Kabaj fullname: Kabaj, M. organization: Wroclaw Medical University – sequence: 6 givenname: B. surname: Karolko fullname: Karolko, B. organization: Wroclaw Medical University – sequence: 7 givenname: J. surname: Maj fullname: Maj, J. organization: Wroclaw Medical University – sequence: 8 givenname: G. surname: Bednarek‐Tupikowska fullname: Bednarek‐Tupikowska, G. organization: Wroclaw Medical University – sequence: 9 givenname: W. surname: Kosmala fullname: Kosmala, W. organization: Wroclaw Medical University – sequence: 10 givenname: J.C. surname: Szepietowski fullname: Szepietowski, J.C. organization: Wroclaw Medical University – sequence: 11 givenname: M. surname: Przewlocka‐Kosmala fullname: Przewlocka‐Kosmala, M. email: monika.przewlocka-kosmala@umed.wroc.pl organization: Wroclaw Medical University |
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CitedBy_id | crossref_primary_10_1111_ijcp_14545 crossref_primary_10_3390_biology11010088 crossref_primary_10_23736_S0391_1977_20_03248_4 crossref_primary_10_3390_biom13101472 crossref_primary_10_1016_j_jaut_2025_103361 crossref_primary_10_3390_metabo12090833 crossref_primary_10_1016_j_jcmg_2019_07_020 crossref_primary_10_3390_ijms21155363 crossref_primary_10_4082_kjfm_20_0053 |
Cites_doi | 10.1111/j.1468-3083.2012.04671.x 10.1021/bi201121m 10.1111/jdv.13152 10.1007/s10067-014-2743-7 10.14712/fb2006052010010 10.1111/bjd.12473 10.1111/j.1600-065X.2009.00794.x 10.1161/ATVBAHA.112.300569 10.1111/j.1600-0625.2011.01261.x 10.1016/j.echo.2014.10.003 10.1159/000341534 10.1111/j.1365-2133.2007.07986.x 10.1111/j.1365-2796.2011.02476.x 10.1023/B:GLYC.0000014084.01324.15 10.1161/01.CIR.0000147181.65298.4D 10.1002/ejhf.113 10.1016/j.acvd.2013.06.054 10.1155/2010/535612 10.1111/j.1365-4632.2012.05584.x 10.1017/S1462399408000719 10.1136/ard.2004.031237 10.1016/j.jchf.2014.08.002 10.1037/0022-3514.51.6.1173 10.1016/j.jaad.2005.04.035 10.1016/j.jacc.2015.10.096 10.1093/ehjci/jew082 10.1016/j.jacc.2012.04.053 10.3892/ijo.25.4.983 10.1111/ijd.12703 10.1016/j.amjmed.2011.03.028 10.1007/s00508-015-0817-4 10.1210/jc.2009-1619 10.1016/j.cjca.2014.11.002 10.1182/blood-2014-04-569939 10.1093/eurjhf/hfp097 10.1016/j.autrev.2008.11.009 10.1016/j.bbagen.2005.12.020 |
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Notes | The authors declare no conflict of interests. This work was financially supported by internal University grant Pbmn127. Conflict of interests Funding ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
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References | 2012; 60 2006; 52 2010; 2010 2015; 3 2015; 127 2015; 125 2004; 25 2015; 31 2013; 106 2013; 169 2016; 30 2005; 64 2006; 1760 2008; 10 2014; 28 2009; 230 2012; 225 2016; 17 2016; 55 2009; 11 2012; 272 2004; 110 2007; 157 2011; 124 2015; 28 2013; 33 2004; 19 1986; 5 2013; 52 2011; 50 2011; 20 2014; 16 2005; 53 2009; 8 2014; 17 2014; 33 2007; 25 2010; 95 2016; 67 e_1_2_6_32_1 e_1_2_6_10_1 e_1_2_6_31_1 Califice S (e_1_2_6_21_1) 2004; 25 e_1_2_6_30_1 Taheri Sarvtin M (e_1_2_6_7_1) 2014; 17 Lee YJ (e_1_2_6_23_1) 2007; 25 Lacina L (e_1_2_6_26_1) 2006; 52 e_1_2_6_19_1 e_1_2_6_13_1 e_1_2_6_36_1 e_1_2_6_14_1 e_1_2_6_35_1 e_1_2_6_11_1 e_1_2_6_34_1 e_1_2_6_12_1 e_1_2_6_33_1 e_1_2_6_17_1 e_1_2_6_18_1 e_1_2_6_39_1 e_1_2_6_15_1 e_1_2_6_38_1 e_1_2_6_16_1 e_1_2_6_37_1 e_1_2_6_20_1 e_1_2_6_40_1 e_1_2_6_9_1 e_1_2_6_8_1 e_1_2_6_5_1 e_1_2_6_4_1 e_1_2_6_6_1 e_1_2_6_25_1 e_1_2_6_24_1 e_1_2_6_3_1 e_1_2_6_2_1 e_1_2_6_22_1 e_1_2_6_29_1 e_1_2_6_28_1 e_1_2_6_27_1 |
References_xml | – volume: 52 start-page: 10 year: 2006 end-page: 15 article-title: Glycophenotype of psoriatic skin publication-title: Folia Biol (Praha) – volume: 106 start-page: 541 year: 2013 end-page: 546 article-title: Galectin‐3: a new biomarker for the diagnosis, analysis and prognosis of acute and chronic heart failure publication-title: Arch Cardiovasc Dis – volume: 169 start-page: 783 year: 2013 end-page: 793 article-title: Psoriasis, psoriatic arthritis and type 2 diabetes mellitus: a systematic review and meta‐analysis publication-title: Br J Dermatol – volume: 127 start-page: 858 year: 2015 end-page: 863 article-title: Assessment of left atrial volume and function in patients with psoriasis by using real time three‐dimensional echocardiography publication-title: Wien Klin Wochenschr – volume: 55 start-page: 158 year: 2016 end-page: 164 article-title: Assessment of subclinical left ventricular dysfunction in patients with psoriasis by speckle tracking echocardiography: A Speckle Tracking Study publication-title: Int J Dermatol – volume: 124 start-page: 775.e1‐6 year: 2011 article-title: Attributable risk estimate of severe psoriasis on major cardiovascular events publication-title: Am J Med – volume: 25 start-page: S41 year: 2007 end-page: S45 article-title: Serum galectin‐3 and galectin‐3 binding protein levels in Behçet's disease and their association with disease activity publication-title: Clin Exp Rheumatol – volume: 28 start-page: 1 year: 2015 end-page: 39.e14 article-title: Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging publication-title: J Am Soc Echocardiogr – volume: 60 start-page: 1249 year: 2012 end-page: 1256 article-title: Galectin‐3, a marker of cardiac fibrosis, predicts incident heart failure in the community publication-title: J Am Coll Cardiol – volume: 157 start-page: 68 year: 2007 end-page: 73 article-title: Prevalence of metabolic syndrome in patients with psoriasis: a hospital‐based case‐control study publication-title: Br J Dermatol – volume: 1760 start-page: 616 year: 2006 end-page: 635 article-title: Galectin‐3: an open‐ended story publication-title: Biochim Biophys Acta – volume: 10 start-page: e17 year: 2008 article-title: Galectins: structure, function and therapeutic potential publication-title: Expert Rev Mol Med – volume: 225 start-page: 88 year: 2012 end-page: 92 article-title: Reduced number of circulating endothelial progenitor cells (CD133+/KDR+) in patients with plaque psoriasis publication-title: Dermatology – volume: 110 start-page: 3121 year: 2004 end-page: 3128 article-title: Galectin‐3 marks activated macrophages in failure‐prone hypertrophied hearts and contributes to cardiac dysfunction publication-title: Circulation – volume: 52 start-page: 153 year: 2013 end-page: 162 article-title: Cardiovascular aspects of psoriasis: an updated review publication-title: Int J Dermatol – volume: 16 start-page: 743 year: 2014 end-page: 748 article-title: Psoriasis and risk of heart failure: a nationwide cohort study publication-title: Eur J Heart Fail – volume: 33 start-page: 1495 year: 2014 end-page: 1500 article-title: Prevalence of cardiovascular risk factors in patients with psoriatic arthritis publication-title: Clin Rheumatol – volume: 33 start-page: 67 year: 2013 end-page: 75 article-title: Galectin‐3 mediates aldosterone‐induced vascular fibrosis publication-title: Arterioscler Thromb Vasc Biol – volume: 125 start-page: 1813 year: 2015 end-page: 1821 article-title: The role of galectin‐3 and galectin‐3‐binding protein in venous thrombosis publication-title: Blood – volume: 17 start-page: 1321 year: 2016 end-page: 1360 article-title: Recommendations for the evaluation of left ventricular diastolic function by echocardiography: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging publication-title: Eur Heart J Cardiovasc Imaging – volume: 3 start-page: 59 year: 2015 end-page: 67 article-title: The impact of galectin‐3 inhibition on aldosterone‐induced cardiac and renal injuries publication-title: JACC Heart Fail – volume: 20 start-page: 303 year: 2011 end-page: 307 article-title: The ‘psoriatic march’: a concept of how severe psoriasis may drive cardiovascular comorbidity publication-title: Exp Dermatol – volume: 67 start-page: 659 year: 2016 end-page: 670 article-title: Contributions of nondiastolic factors to exercise intolerance in heart failure with preserved ejection fraction publication-title: J Am Coll Cardiol – volume: 50 start-page: 7842 year: 2011 end-page: 7857 article-title: When galectins recognize glycans: from biochemistry to physiology and back again publication-title: Biochemistry – volume: 272 start-page: 55 year: 2012 end-page: 64 article-title: The fibrosis marker galectin‐3 and outcome in the general population publication-title: J Intern Med – volume: 8 start-page: 360 year: 2009 end-page: 363 article-title: The immunological potential of galectin‐1 and ‐3 publication-title: Autoimmun Rev – volume: 95 start-page: 1404 year: 2010 end-page: 1411 article-title: Serum galectin‐3 is elevated in obesity and negatively correlates with glycosylated hemoglobin in type 2 diabetes publication-title: J Clin Endocrinol Metab – volume: 19 start-page: 543 year: 2004 end-page: 549 article-title: Galectin‐3 and metastasis publication-title: Glycoconj J – volume: 5 start-page: 1173 year: 1986 end-page: 1182 article-title: The moderator‐mediator variable distinction in social psychological research: conceptual, strategic, and statistical considerations publication-title: J Pers Soc Psychol – volume: 230 start-page: 160 year: 2009 end-page: 171 article-title: The regulation of inflammation by galectin‐3 publication-title: Immunol Rev – volume: 2010 year: 2010 article-title: Lipid disturbances in psoriasis: an update publication-title: Mediators Inflamm – volume: 30 start-page: 819 year: 2016 end-page: 823 article-title: Myocardial function and effects of biologic therapy in patients with severe psoriasis: a prospective echocardiographic study publication-title: J Eur Acad Dermatol Venereol – volume: 64 start-page: ii65 issue: Suppl 2 year: 2005 end-page: ii68 article-title: Psoriasis assessment tools in clinical trials publication-title: Ann Rheum Dis – volume: 28 start-page: 116 year: 2014 end-page: 119 article-title: Increased number of circulating endothelial cells (CECs) in patients with psoriasis–preliminary report publication-title: J Eur Acad Dermatol Venereol – volume: 11 start-page: 811 year: 2009 end-page: 817 article-title: Galectin‐3: a novel mediator of heart failure development and progression publication-title: Eur J Heart Fail – volume: 25 start-page: 983 year: 2004 end-page: 992 article-title: Galectin‐3 and cancer (Review) publication-title: Int J Oncol – volume: 31 start-page: 287 year: 2015 end-page: 295 article-title: Similarities in coronary function and myocardial deformation between psoriasis and coronary artery disease: the role of oxidative stress and inflammation publication-title: Can J Cardiol – volume: 53 start-page: S94 year: 2005 end-page: S100 article-title: Psoriasis–recent advances in understanding its pathogenesis and treatment publication-title: J Am Acad Dermatol – volume: 17 start-page: 343 year: 2014 end-page: 346 article-title: Serum lipids and lipoproteins in patients with psoriasis publication-title: Arch Iran Med – ident: e_1_2_6_3_1 doi: 10.1111/j.1468-3083.2012.04671.x – ident: e_1_2_6_38_1 doi: 10.1021/bi201121m – volume: 25 start-page: S41 year: 2007 ident: e_1_2_6_23_1 article-title: Serum galectin‐3 and galectin‐3 binding protein levels in Behçet's disease and their association with disease activity publication-title: Clin Exp Rheumatol – ident: e_1_2_6_16_1 doi: 10.1111/jdv.13152 – ident: e_1_2_6_9_1 doi: 10.1007/s10067-014-2743-7 – volume: 52 start-page: 10 year: 2006 ident: e_1_2_6_26_1 article-title: Glycophenotype of psoriatic skin publication-title: Folia Biol (Praha) doi: 10.14712/fb2006052010010 – ident: e_1_2_6_5_1 doi: 10.1111/bjd.12473 – ident: e_1_2_6_20_1 doi: 10.1111/j.1600-065X.2009.00794.x – ident: e_1_2_6_31_1 doi: 10.1161/ATVBAHA.112.300569 – ident: e_1_2_6_8_1 doi: 10.1111/j.1600-0625.2011.01261.x – ident: e_1_2_6_28_1 doi: 10.1016/j.echo.2014.10.003 – ident: e_1_2_6_4_1 doi: 10.1159/000341534 – ident: e_1_2_6_6_1 doi: 10.1111/j.1365-2133.2007.07986.x – ident: e_1_2_6_34_1 doi: 10.1111/j.1365-2796.2011.02476.x – ident: e_1_2_6_22_1 doi: 10.1023/B:GLYC.0000014084.01324.15 – ident: e_1_2_6_37_1 doi: 10.1161/01.CIR.0000147181.65298.4D – ident: e_1_2_6_13_1 doi: 10.1002/ejhf.113 – ident: e_1_2_6_35_1 doi: 10.1016/j.acvd.2013.06.054 – ident: e_1_2_6_11_1 doi: 10.1155/2010/535612 – ident: e_1_2_6_12_1 doi: 10.1111/j.1365-4632.2012.05584.x – ident: e_1_2_6_18_1 doi: 10.1017/S1462399408000719 – ident: e_1_2_6_27_1 doi: 10.1136/ard.2004.031237 – ident: e_1_2_6_32_1 doi: 10.1016/j.jchf.2014.08.002 – ident: e_1_2_6_30_1 doi: 10.1037/0022-3514.51.6.1173 – ident: e_1_2_6_2_1 doi: 10.1016/j.jaad.2005.04.035 – ident: e_1_2_6_36_1 doi: 10.1016/j.jacc.2015.10.096 – ident: e_1_2_6_29_1 doi: 10.1093/ehjci/jew082 – ident: e_1_2_6_33_1 doi: 10.1016/j.jacc.2012.04.053 – volume: 17 start-page: 343 year: 2014 ident: e_1_2_6_7_1 article-title: Serum lipids and lipoproteins in patients with psoriasis publication-title: Arch Iran Med – volume: 25 start-page: 983 year: 2004 ident: e_1_2_6_21_1 article-title: Galectin‐3 and cancer (Review) publication-title: Int J Oncol doi: 10.3892/ijo.25.4.983 – ident: e_1_2_6_14_1 doi: 10.1111/ijd.12703 – ident: e_1_2_6_10_1 doi: 10.1016/j.amjmed.2011.03.028 – ident: e_1_2_6_15_1 doi: 10.1007/s00508-015-0817-4 – ident: e_1_2_6_24_1 doi: 10.1210/jc.2009-1619 – ident: e_1_2_6_39_1 doi: 10.1016/j.cjca.2014.11.002 – ident: e_1_2_6_40_1 doi: 10.1182/blood-2014-04-569939 – ident: e_1_2_6_25_1 doi: 10.1093/eurjhf/hfp097 – ident: e_1_2_6_19_1 doi: 10.1016/j.autrev.2008.11.009 – ident: e_1_2_6_17_1 doi: 10.1016/j.bbagen.2005.12.020 |
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Psoriasis has been shown to increase cardiovascular risk, and a contributor to this might be enhanced myocardial fibrosis promoted by the... Psoriasis has been shown to increase cardiovascular risk, and a contributor to this might be enhanced myocardial fibrosis promoted by the disease-associated... |
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SubjectTerms | Adult Aged Asymptomatic Diseases Blood Sedimentation C-Reactive Protein - metabolism Case-Control Studies Diastole Echocardiography Female Galectin 3 - blood Humans Male Middle Aged Psoriasis - blood Systole Ventricular Dysfunction, Left - blood Ventricular Dysfunction, Left - diagnostic imaging Ventricular Dysfunction, Left - physiopathology Waist Circumference Waist-Height Ratio |
Title | Role of galectin‐3 in subclinical myocardial impairment in psoriasis |
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