Galectin-1 controls cardiac inflammation and ventricular remodeling during acute myocardial infarction

Am J Pathol. 2013 Jan;182(1):29-40. doi: 10.1016/j.ajpath.2012.09.022. Epub 2012 Nov 9.


Galectin-1 (Gal-1), an evolutionarily conserved β-galactoside-binding lectin, plays essential roles in the control of inflammation and neovascularization. Although identified as a major component of the contractile apparatus of cardiomyocytes, the potential role of Gal-1 in modulating heart pathophysiology is uncertain. Here, we aimed to characterize Gal-1 expression and function in the infarcted heart. Expression of Gal-1 was substantially increased in the mouse heart 7 days after acute myocardial infarction (AMI) and in hearts from patients with end-stage chronic heart failure. This lectin was localized mainly in cardiomyocytes and inflammatory infiltrates in peri-infarct areas, but not in remote areas. Both simulated hypoxia and proinflammatory cytokines selectively up-regulated Gal-1 expression in mouse cardiomyocytes, whereas anti-inflammatory cytokines inhibited expression of this lectin or had no considerable effect. Compared with their wild-type counterpart, Gal-1-deficient (Lgals1(-/-)) mice showed enhanced cardiac inflammation, characterized by increased numbers of macrophages, natural killer cells, and total T cells, but reduced frequency of regulatory T cells, leading to impaired cardiac function at baseline and impaired ventricular remodeling 7 days after nonreperfused AMI. Treatment of mice with recombinant Gal-1 attenuated cardiac damage in reperfused AMI. Taken together, our results indicate a protective role for Gal-1 in normal cardiac homeostasis and postinfarction remodeling by preventing cardiac inflammation. Thus, Gal-1 treatment represents a potential novel strategy to attenuate heart failure in AMI.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Animals
  • Apoptosis / drug effects
  • Apoptosis / physiology
  • Cell Hypoxia / physiology
  • Cells, Cultured
  • Cytokines / pharmacology
  • Female
  • Galectin 1 / biosynthesis
  • Galectin 1 / pharmacology
  • Galectin 1 / physiology*
  • Galectin 1 / therapeutic use
  • Heart Failure / metabolism
  • Heart Failure / physiopathology
  • Heart Rate / drug effects
  • Heart Rate / physiology
  • Humans
  • Inflammation Mediators / pharmacology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Middle Aged
  • Myocardial Infarction / complications
  • Myocardial Infarction / drug therapy
  • Myocardial Infarction / metabolism
  • Myocardial Infarction / physiopathology*
  • Myocarditis / etiology
  • Myocarditis / metabolism*
  • Myocytes, Cardiac / drug effects
  • Myocytes, Cardiac / metabolism
  • Recombinant Proteins / therapeutic use
  • Up-Regulation / drug effects
  • Up-Regulation / physiology
  • Ventricular Function, Left / physiology
  • Ventricular Remodeling / physiology*
  • Young Adult


  • Cytokines
  • Galectin 1
  • Inflammation Mediators
  • Recombinant Proteins