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Letter to the Editor| Volume 163, ISSUE 3, P335-337, March 10, 2013

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Galectin-3: Relation to infarct scar and left ventricular function after myocardial infarction

      Elevated serum levels of galectin-3, a member of the lectin family, have recently been reported in heart failure patients, as well as in animal models of heart failure [
      • de Boer R.A.
      • Voors A.A.
      • Muntendam P.
      • van Gilst W.H.
      • van Veldhuisen D.J.
      Galectin-3: a novel mediator of heart failure development and progression.
      ,
      • Sharma U.C.
      • Pokharel S.
      • van Brakel T.L.
      • et al.
      Galectin-3 marks activated macrophages in failure-prone hypertrophied hearts and contributes to cardiac dysfunction.
      ,
      • Sharma U.
      • Rhaleb N.E.
      • Pokharel S.
      • et al.
      Novel anti-inflammatory mechanisms of N-Acetyl-Ser-Asp-Lys-Pro in hypertension-induced target organ damage.
      • Conroy R.M.
      • Pyörälä K.
      • Fitzgerald A.P.
      987–1003
      Estimation of ten-year risk of fatal cardiovascular disease in Europe: the SCORE project.
      ]. Apart from cardiac remodelling, upregulation of galectin-3 expression and release has also been associated with several other human fibrotic conditions including liver cirrhosis, idiopathic lung fibrosis, pancreatitis and renal failure. Therefore, this lectin is thought to play some regulatory role between inflammation and fibrosis [
      • de Boer R.A.
      • Voors A.A.
      • Muntendam P.
      • van Gilst W.H.
      • van Veldhuisen D.J.
      Galectin-3: a novel mediator of heart failure development and progression.
      ]. Its direct mediation of profibrotic pathways such as cell adhesion and proliferation suggests that galectin-3 is involved in the development of heart failure [
      • Dumic J.
      • Dabelic S.
      • Flögel M.
      Galectin-3: an open-ended story.
      ,
      • Yang R.Y.
      • Rabinovich G.A.
      • Liu F.T.
      Galectins: structure, function and therapeutic potential.
      ]. After acute myocardial infarction (AMI), fibrosis and tissue remodelling are the leading causes for the development of heart failure.

      Keywords

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