Galectin-1 as an Emerging Mediator of Cardiovascular Inflammation: Mechanisms and Therapeutic Opportunities

<div>Role of Gal-1 in acute myocardial infarction. (a) Gal-1 is constitutively expressed in cardiomyocytes close to sarcomeric actin and is increased and secreted after acute myocardial infarction (AMI), inflammation, and hypoxia. (b) Mice lacking Gal-1 (<i>Lgals1<sup>−/−</sup></i>) show adverse ventricular remodeling after AMI associated with increased inflammation and reduced proportion of regulatory T (Treg) cells.</div>

Mediators of Inflammation

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Figure 1

Figure 1: Galectin-1 as an Emerging Mediator of Cardiovascular Inflammation: Mechanisms and Therapeutic Opportunities 