{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T20:38:37Z","timestamp":1791923917183,"version":"4.3.4"},"reference-count":45,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2013,1]]},"abstract":"<jats:sec>\n                    <jats:title>Objective\u2014<\/jats:title>\n                    <jats:p>Aldosterone (Aldo) is involved in arterial stiffness and heart failure, but the mechanisms have remained unclear. Galectin-3 (Gal-3), a \u03b2-galactoside-binding lectin, plays an important role in inflammation, fibrosis, and heart failure. We investigated here whether Gal-3 is involved in Aldo-induced vascular fibrosis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and Results\u2014<\/jats:title>\n                    <jats:p>In rat vascular smooth muscle cells Gal-3 overexpression enhanced specifically collagen type I synthesis. Moreover Gal-3 inhibition by modified citrus pectin or small interfering RNA blocked Aldo-induced collagen type I synthesis. Rats were treated with Aldo-salt combined with spironolactone or modified citrus pectin for 3 weeks. Hypertensive Aldo-treated rats presented vascular hypertrophy, inflammation, fibrosis, and increased aortic Gal-3 expression. Spironolactone or modified citrus pectin treatment reversed all the above effects. Wild-type and Gal-3 knock-out mice were treated with Aldo for 6 hours or 3 weeks. Aldo increased aortic Gal-3 expression, inflammation, and collagen type I in wild-type mice at both the short- and the long-term, whereas no changes occurred in Gal-3 knock-out mice.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion\u2014<\/jats:title>\n                    <jats:p>Our data indicate that Gal-3 is required for inflammatory and fibrotic responses to Aldo in vascular smooth muscle cells in vitro and in vivo, suggesting a key role for Gal-3 in vascular fibrosis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/atvbaha.112.300569","type":"journal-article","created":{"date-parts":[[2012,11,2]],"date-time":"2012-11-02T20:24:29Z","timestamp":1351887869000},"page":"67-75","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":330,"title":["Galectin-3 Mediates Aldosterone-Induced Vascular 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CNRS, Universit\u00e9 de Lorraine UMR 7561 (P.R.), Vandoeuvre-L\u00e8s-Nancy, F-54500, France; Department of Cardiology, University Medical Center Groningen, University of Groningen (d.B.R.A), Groningen, The Netherlands; CNRS, Paris-Diderot University, UMR 7592 (F.P.), Paris, F-75000, France; CHU Nancy, Inserm Clinical..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pascal","family":"Reboul","sequence":"additional","affiliation":[{"name":"From the INSERM, Universit\u00e9 de Lorraine UMR 961 (L.C., P.L., F.Z., P.R., N.L-A.), Vandoeuvre-L\u00e8s-Nancy, F-54500, France; Universidad complutense de Madrid (M.M., V.C., E.M-M.), Madrid, Spain; CNRS, Universit\u00e9 de Lorraine UMR 7561 (P.R.), Vandoeuvre-L\u00e8s-Nancy, F-54500, France; Department of Cardiology, University Medical Center Groningen, University of Groningen (d.B.R.A), Groningen, The Netherlands; CNRS, Paris-Diderot University, UMR 7592 (F.P.), Paris, F-75000, France; CHU Nancy, Inserm 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(M.M., V.C., E.M-M.), Madrid, Spain; CNRS, Universit\u00e9 de Lorraine UMR 7561 (P.R.), Vandoeuvre-L\u00e8s-Nancy, F-54500, France; Department of Cardiology, University Medical Center Groningen, University of Groningen (d.B.R.A), Groningen, The Netherlands; CNRS, Paris-Diderot University, UMR 7592 (F.P.), Paris, F-75000, France; CHU Nancy, Inserm Clinical..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rudolf A.","family":"de Boer","sequence":"additional","affiliation":[{"name":"From the INSERM, Universit\u00e9 de Lorraine UMR 961 (L.C., P.L., F.Z., P.R., N.L-A.), Vandoeuvre-L\u00e8s-Nancy, F-54500, France; Universidad complutense de Madrid (M.M., V.C., E.M-M.), Madrid, Spain; CNRS, Universit\u00e9 de Lorraine UMR 7561 (P.R.), Vandoeuvre-L\u00e8s-Nancy, F-54500, France; Department of Cardiology, University Medical Center Groningen, University of Groningen (d.B.R.A), Groningen, The Netherlands; CNRS, Paris-Diderot University, UMR 7592 (F.P.), Paris, F-75000, France; CHU Nancy, Inserm Clinical..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fran\u00e7oise","family":"Poirier","sequence":"additional","affiliation":[{"name":"From the INSERM, Universit\u00e9 de Lorraine UMR 961 (L.C., P.L., F.Z., P.R., N.L-A.), Vandoeuvre-L\u00e8s-Nancy, F-54500, France; Universidad complutense de Madrid (M.M., V.C., E.M-M.), Madrid, Spain; CNRS, Universit\u00e9 de Lorraine UMR 7561 (P.R.), Vandoeuvre-L\u00e8s-Nancy, F-54500, France; Department of Cardiology, University Medical Center Groningen, University of Groningen (d.B.R.A), Groningen, The Netherlands; CNRS, Paris-Diderot University, UMR 7592 (F.P.), Paris, F-75000, France; CHU Nancy, Inserm Clinical..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patrick","family":"Lacolley","sequence":"additional","affiliation":[{"name":"From the INSERM, Universit\u00e9 de Lorraine UMR 961 (L.C., P.L., F.Z., P.R., N.L-A.), Vandoeuvre-L\u00e8s-Nancy, F-54500, France; Universidad complutense 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