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...
Saved in:
Main Authors: | , , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
Wiley
2018-01-01
|
Series: | Mediators of Inflammation |
Online Access: | http://dx.doi.org/10.1155/2018/8696543 |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
_version_ | 1832552492624248832 |
---|---|
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. |
format | Article |
id | doaj-art-4135328507c6443db4d01c9200ebd0d0 |
institution | Kabale University |
issn | 0962-9351 1466-1861 |
language | English |
publishDate | 2018-01-01 |
publisher | Wiley |
record_format | Article |
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 |
work_keys_str_mv | AT ignaciomseropian galectin1asanemergingmediatorofcardiovascularinflammationmechanismsandtherapeuticopportunities AT germanegonzalez galectin1asanemergingmediatorofcardiovascularinflammationmechanismsandtherapeuticopportunities AT sebastianmmaller galectin1asanemergingmediatorofcardiovascularinflammationmechanismsandtherapeuticopportunities AT danielhberrocal galectin1asanemergingmediatorofcardiovascularinflammationmechanismsandtherapeuticopportunities AT antonioabbate galectin1asanemergingmediatorofcardiovascularinflammationmechanismsandtherapeuticopportunities AT gabrielarabinovich galectin1asanemergingmediatorofcardiovascularinflammationmechanismsandtherapeuticopportunities |