Central role of Galectin-3 at the cross-roads of cardiac inflammation and fibrosis: implications for heart failure and transplantation
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...
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| Autores principales: | , , , , |
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| Formato: | Artículo |
| Lenguaje: | Inglés |
| Publicado: |
Elsevier
2025
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| Acceso en línea: | https://repositorio.uca.edu.ar/handle/123456789/20020 |
| Aporte de: |
| Sumario: | 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. |
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