Limited ability of the heart to regenerate aggravates myocardial infarction (MI), a major cause of heart failure. Galectin-1, an endogenous β-galactoside-binding lectin, accelerates heart regenerative and repair responses following MI by modulating immunological responses, promoting angiogenesis, and improving cell survival. Galectin-1 is associated with cardiomyocytes (CMs) survival by activating the PI3K/AKT signaling pathway and facilitates limited adverse remodeling by switching to M2 macrophages. The upregulation of Galectin-in response to ischemia-induced inflammation and hypoxia highlights its function in endogenous defense systems. Galectin-1 is critical in cardiac regeneration due to the synergistic immunomodulatory, angiogenic, and electrophysiological effects. Even though recent reports highlight importance of Galectin-1 in cardio protection, mechanistic investigations, and translational/clinical studies are limited. This article focuses on a comprehensive review on the current understanding regarding the cardioprotective effects and translational opportunities of Galectin-1 for the management of MI.
Luo et al. (Sat,) studied this question.