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Título: Central role of Galectin-3 at the cross-roads of cardiac inflammation and fibrosis: implications for heart failure and transplantation
Autor: Seropian, Ignacio M. 
El-Diasty, Mohammad 
El-Sherbini, Adham H. 
González, Germán E. 
Rabinovich, Gabriel A. 
Palabras clave: SISTEMA CARDIOVASCULARINSUFICIENCIA CARDIACAFIBROSISTRANSPLANTE DE ORGANOSGALECTIN 3
Fecha de publicación: 2024
Editorial: Elsevier
Resumen: Cardiac inflammation and fibrosis are central pathogenic mechanisms leading to heart failure. Transplantation is still the treatment of choice for many patients undergoing end-stage heart failure who remain symptomatic despite optimal medical therapy. In spite of considerable progress, the molecular mechanisms linking inflammation, fibrosis and heart failure remain poorly understood. Galectin-3 (GAL3), a chimera-type member of the galectin family, has emerged as a critical mediator implicated in cardiac inflammatory, vascular and fibrotic processes through modulation of different cellular compartments including monocytes and macrophages, fibroblasts, endothelial cells and vascular smooth muscle cells via glycan-dependent or independent mechanisms. GAL3-driven circuits may hierarchically amplify cytokine production and function, immune cell activation and fibrosis cascades, influencing a wide range of cardiovascular disorders. Thus, GAL3 emerges as a potential therapeutic target to counteract aberrant inflammation and fibrosis during heart failure and a potential biomarker of heart failure and clinical outcome of heart transplantation.
URI: https://repositorio.uca.edu.ar/handle/123456789/20020
DOI: 10.1016/j.cytogfr.2024.10.002
Derechos: Atribución-NoComercial-CompartirIgual 4.0 Internacional
Fuente: Cytokine and Growth Factor Reviews. 80, 2024.
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