GALECTIN-1 AS AN EMERGING MEDIATOR OF CARDIOVASCULAR INFLAMMATION: MECHANISMS AND THERAPEUTIC OPPORTUNITIES

IGNACIO M. SEROPIAN; GERMÁN E. GONZALEZ; SEBASTIÁN M. MALLER; DANIEL H. BERROCAL; ANTONIO ABBATE; GABRIEL A. RABINOVICH

MEDIATORS OF INFLAMMATION

HINDAWI PUBLISHING CORPORATION

Lugar: New York; Año: 2018 vol. 2018 p. 8696543 - 8696554

0962-9351

Galectin-1 (Gal-1), an evolutionarily conserved beta-galactoside-binding lectin, controls immune cell homeostasis and tempers acute and chronic inflammation by blunting pro-inflammatory cytokine synthesis, engaging T-cell apoptotic programs, promoting expansion of T regulatory (Treg) cells and de-activating antigen-presenting cells. In addition, this lectin promotes angiogenesis by co-opting the vascular endothelial growth factor receptor (VEGFR)2 signaling pathway. Since a coordinated network of immunomodulatory and pro-angiogenic mediators controls cardiac homeostasis, this lectin has been proposed to play a key hierarchical role in cardiac pathophysiology via glycan-dependent regulation of inflammatory responses. Here we discuss the emerging roles of Gal-1 in cardiovascular diseases including acute myocardial infarction, heart failure, Chagas cardiomyopathy, pulmonary hypertension and ischemic stroke, highlighting underlying anti-inflammatory mechanisms and therapeutic opportunities. Whereas Gal-1 administration emerges as a potential novel treatment option in acute myocardial infarction and ischemic stroke, Gal-1 blockade may contribute to attenuate pulmonary arterial hypertension. Keywords: galectin-1; cardiovascular diseases; acute myocardial infarction; heart failure; stroke; pulmonary hypertension