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Unraveling the role of galectin-3 in cardiac pathology and physiology

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dc.contributor.authorSeropian, Ignacio M.
dc.contributor.authorCassaglia, Pablo
dc.contributor.authorMiksztowicz, Verónica
dc.contributor.authorGonzález, Germán E.
dc.date.accessioned2025-02-04T23:15:49Z
dc.date.available2025-02-04T23:15:49Z
dc.date.issued2023
dc.description.abstractGalectin-3 (Gal-3) is a carbohydrate-binding protein with multiple functions. Gal-3 regulates cell growth, proliferation, and apoptosis by orchestrating cell-cell and cell-matrix interactions. It is implicated in the development and progression of cardiovascular disease, and its expression is increased in patients with heart failure. In atherosclerosis, Gal-3 promotes monocyte recruitment to the arterial wall boosting inflammation and atheroma. In acute myocardial infarction (AMI), the expression of Gal-3 increases in infarcted and remote zones from the beginning of AMI, and plays a critical role in macrophage infiltration, differentiation to M1 phenotype, inflammation and interstitial fibrosis through collagen synthesis. Genetic deficiency of Gal-3 delays wound healing, impairs cardiac remodeling and function after AMI. On the contrary, Gal-3 deficiency shows opposite results with improved remodeling and function in other cardiomyopathies and in hypertension. Pharmacologic inhibition with non-selective inhibitors is also protective in cardiac disease. Finally, we recently showed that Gal-3 participates in normal aging. However, genetic absence of Gal-3 in aged mice exacerbates pathological hypertrophy and increases fibrosis, as opposed to reduced fibrosis shown in cardiac disease. Despite some gaps in understanding its precise mechanisms of action, Gal-3 represents a potential therapeutic target for the treatment of cardiovascular diseases and the management of cardiac aging. In this review, we summarize the current knowledge regarding the role of Gal-3 in the pathophysiology of heart failure, atherosclerosis, hypertension, myocarditis, and ischemic heart disease. Furthermore, we describe the physiological role of Gal-3 in cardiac aging.eng
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dc.identifier.citationSeropian IM, Cassaglia P, Miksztowicz V and González GE (2023) Unraveling the role of galectin-3 in cardiac pathology and physiology. Front. Physiol. 14:1304735.
dc.identifier.doihttps://doi.org/10.3389/fphys.2023.1304735
dc.identifier.urihttps://repositorio.unahur.edu.ar/handle/123456789/735
dc.identifier.urihttps://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2023.1304735/full
dc.journal.titleFrontiers in Physiology
dc.journal.volume14
dc.language.isoeng
dc.rights.licenseinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/
dc.subject.ocde1Ciencias Médicas y de Salud
dc.subject.ocde2Medicina Clínica
dc.subject.unahurUna salud. Comunitaria
dc.titleUnraveling the role of galectin-3 in cardiac pathology and physiology
dc.typeinfo:eu-repo/semantics/article
dc.type.oaireinfo:eu-repo/semantics/article
dc.type.snrdinfo:ar-repo/semantics/artículo
dc.type.versioninfo:eu-repo/semantics/publishedVersion
dspace.entity.typePublication
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