Galectin-3, Cardiac Function, and Fibrosis

Wouter C Meijers; Natalia López-Andrés; Rudolf A de Boer

doi:10.1016/j.ajpath.2016.05.002

Galectin-3, Cardiac Function, and Fibrosis

Am J Pathol. 2016 Aug;186(8):2232-2234. doi: 10.1016/j.ajpath.2016.05.002. Epub 2016 Jul 20.

Authors

Wouter C Meijers¹, Natalia López-Andrés², Rudolf A de Boer³

Affiliations

¹ Department of Cardiology, University Medical Center Groningen, University of Groningen, RB Groningen, the Netherlands.
² Cardiovascular Translational Research, Sanataria de Navarra Research Institute, Pamplona, Spain.
³ Department of Cardiology, University Medical Center Groningen, University of Groningen, RB Groningen, the Netherlands. Electronic address: r.a.de.boer@umcg.nl.

PMID: 27461364
DOI: 10.1016/j.ajpath.2016.05.002

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).

Publication types

Letter
Comment

MeSH terms

Fibrosis*
Galectin 3*
Heart
Humans
Myocardium
Ventricular Remodeling

Substances

Galectin 3