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

Galectin-1 (Gal-1), an evolutionarily conserved β-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 deactiva...

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Main Authors: Ignacio M. Seropian, Germán E. González, Sebastián M. Maller, Daniel H. Berrocal, Antonio Abbate, Gabriel A. Rabinovich
Format: Article
Language:English
Published: Wiley 2018-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2018/8696543
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author Ignacio M. Seropian
Germán E. González
Sebastián M. Maller
Daniel H. Berrocal
Antonio Abbate
Gabriel A. Rabinovich
author_facet Ignacio M. Seropian
Germán E. González
Sebastián M. Maller
Daniel H. Berrocal
Antonio Abbate
Gabriel A. Rabinovich
author_sort Ignacio M. Seropian
collection DOAJ
description Galectin-1 (Gal-1), an evolutionarily conserved β-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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issn 0962-9351
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publishDate 2018-01-01
publisher Wiley
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series Mediators of Inflammation
spelling doaj-art-4135328507c6443db4d01c9200ebd0d02025-02-03T05:58:34ZengWileyMediators of Inflammation0962-93511466-18612018-01-01201810.1155/2018/86965438696543Galectin-1 as an Emerging Mediator of Cardiovascular Inflammation: Mechanisms and Therapeutic OpportunitiesIgnacio M. Seropian0Germán E. González1Sebastián M. Maller2Daniel H. Berrocal3Antonio Abbate4Gabriel A. Rabinovich5Servicio de Hemodinamia y Cardiología Intervencionista, Instituto de Medicina Cardiovascular, Hospital Italiano de Buenos Aires, Buenos Aires C1199, ArgentinaInstituto de Biología y Medicina Molecular, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Instituto de Fisiopatología Cardiovascular, Departamento de Patología, Universidad de Buenos Aires, Buenos Aires C1428, ArgentinaLaboratorio de Inmunopatología, Instituto de Biología y Medicina Experimental (IBYME), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Buenos Aires C1428, ArgentinaServicio de Hemodinamia y Cardiología Intervencionista, Instituto de Medicina Cardiovascular, Hospital Italiano de Buenos Aires, Buenos Aires C1199, ArgentinaPauley Heart Center, Virginia Commonwealth University, Richmond, VA 23298, USALaboratorio de Inmunopatología, Instituto de Biología y Medicina Experimental (IBYME), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Buenos Aires C1428, ArgentinaGalectin-1 (Gal-1), an evolutionarily conserved β-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.http://dx.doi.org/10.1155/2018/8696543
spellingShingle Ignacio M. Seropian
Germán E. González
Sebastián M. Maller
Daniel H. Berrocal
Antonio Abbate
Gabriel A. Rabinovich
Galectin-1 as an Emerging Mediator of Cardiovascular Inflammation: Mechanisms and Therapeutic Opportunities
Mediators of Inflammation
title Galectin-1 as an Emerging Mediator of Cardiovascular Inflammation: Mechanisms and Therapeutic Opportunities
title_full Galectin-1 as an Emerging Mediator of Cardiovascular Inflammation: Mechanisms and Therapeutic Opportunities
title_fullStr Galectin-1 as an Emerging Mediator of Cardiovascular Inflammation: Mechanisms and Therapeutic Opportunities
title_full_unstemmed Galectin-1 as an Emerging Mediator of Cardiovascular Inflammation: Mechanisms and Therapeutic Opportunities
title_short Galectin-1 as an Emerging Mediator of Cardiovascular Inflammation: Mechanisms and Therapeutic Opportunities
title_sort galectin 1 as an emerging mediator of cardiovascular inflammation mechanisms and therapeutic opportunities
url http://dx.doi.org/10.1155/2018/8696543
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