Galectin-3, Cardiac Function, and Fibrosis

descriptionPublicationkeyboard_double_arrow_right Article 01 Aug 2016 Netherlands English Publisher:Elsevier BVJournal:The American Journal of Pathology, volume 186, pages 2,232-2,234 (issn: 0002-9440,

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Authors: Meijers, Wouter C.; Lopez-Andres, Natalia; de Boer, Rudolf A.;

doi: 10.1016/j.ajpath.2016.05.002

pmid: 27461364

handle: 11370/cb883e6e-29b9-4539-9eec-7867258e227c

Galectin-3, Cardiac Function, and Fibrosis

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Abstract

This Correspondence relates to the article by Frunza et al (Myocardial Galectin-3 Expression Is Associated with Remodeling of the Pressure-Overloaded Heart and May Delay the Hypertrophic Response without Affecting Survival, Dysfunction, and Cardiac Fibrosis. Am J Pathol 2016, 186:1114-1127).

Country

Netherlands

Related Organizations

University Medical Center Groningen
Netherlands
University of Groningen
Netherlands

Keywords

Ventricular Remodeling, Galectin 3, Myocardium, INHIBITION, INJURY, Humans, Heart, GALECTIN-3/AGE-RECEPTOR-3 KNOCKOUT MICE, Fibrosis

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