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Review
. 2024 Dec:80:47-58.
doi: 10.1016/j.cytogfr.2024.10.002. Epub 2024 Oct 20.

Central role of Galectin-3 at the cross-roads of cardiac inflammation and fibrosis: Implications for heart failure and transplantation

Ignacio M Seropian  1 , Mohammad El-Diasty  2 , Adham H El-Sherbini  3 , Germán E González  4 , Gabriel A Rabinovich  5
Affiliations
Review

Central role of Galectin-3 at the cross-roads of cardiac inflammation and fibrosis: Implications for heart failure and transplantation

Ignacio M Seropian et al. Cytokine Growth Factor Rev. 2024 Dec.

Abstract

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.

Keywords: Cardiac physiopathology; Fibrosis; Galectin-3; Heart failure; Inflammation; Transplantation.

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Conflict of interest statement

Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests Gabriel A. Rabinovich reports financial support was provided by Argentina Ministry of Science Technology and Innovation. Gabriel A. Rabinovich reports financial support was provided by National Agency for the Promotion of Research Technological Development and Innovation. Gabriel A. Rabinovich reports financial support was provided by Fundación Sales. Gabriel A. Rabinovich reports financial support was provided by Bunge y Born Foundation. Gabriel A. Rabinovich reports financial support was provided by Rene Baron Foundation. German E. Gonzalez reports financial support was provided by National Agency for the Promotion of Scientific Research. German E. Gonzalez reports financial support was provided by National Scientific and Technical Research Council. Gabriel A. Rabinovich reports a relationship with GALTEC that includes: equity or stocks. No additional relationships or activities If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

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