Possible value of galectin‐3 on follow‐up of cardiac remodeling during glucocorticoid treatment

Abstract

Glucocorticoids are among the most prescribed drugs globally due to their potent anti‐inflammatory and immunosuppressive properties. Although they have positive effects on the treatment of various disease states; long‐term administration is associated with high blood pressure, insulin resistance, and susceptibility to type 2 diabetes. The heart attempts to cope with increased blood pressure and a decrease in glucose utilization by developing pathological cardiac remodeling. However, in this process, cardiac fibrosis formation and deterioration in heart structure and functions occur. Galectin‐3, a member of the β‐galactoside binding lectins, is consistently associated with inflammation and fibrosis in the pathogenesis of various disease states including insulin resistance and heart failure. Galectin‐3 expression is markedly increased in activated macrophages and a subset of activated fibroblasts and vascular cells. Also, failing and remodeling myocardium show increased Gal‐3 expression and elevated Gal‐3 levels are related to heart failure severity and prognosis. Furthermore, Gal‐3‐related pathways are recently suggested as therapeutic targets both pharmacologically and genetically to increase insulin sensitivity in vivo. The objective of this review is to provide a summary of our current understanding of the role of glucocorticoid‐associated insulin resistance, which is important for some cardiac events, and the potential role of galectin in this pathophysiological process.