Journal
MEDIATORS OF INFLAMMATION
Volume 2018, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2018/8696543
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Funding
- Argentinean Agency for Promotion of Science and Technology [PICT V 2014-367, 2014-2320]
- Bunge & Born Foundation
- University of Buenos Aires Science and Technology [UBACyT 20020170100619BA]
- Allende Foundation
- National Academy of Medicine of Argentina
- National Heart, Lung, and Blood Institute, Bethesda, Maryland, USA [HL121402, HL136816]
- Hospital Italiano de Buenos Aires
- Sales Foundation
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Galectin-1 (Gal-1), an evolutionarily conserved beta-galactoside-binding lectin, controls immune cell homeostasis and tempers acute and chronic inflammation by blunting proinflammatory cytokine synthesis, engaging T-cell apoptotic programs, promoting expansion of T regulatory (Treg) cells, and deactivating 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 proangiogenic 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.
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