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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 CARDIOVASCULAR; INSUFICIENCIA CARDIACA; FIBROSIS; TRANSPLANTE DE ORGANOS; GALECTIN 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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