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Galectin-3 and fibrosis intensity in Chronic Chagas Cardiomyopathy: a systematic review
Ana Thereza Chaves1, Ana Laura Grossi de Oliveira1, Nathalia Sernizon Guimarães1
1Universidade Federal de Minas Gerais, Faculdade de Medicina, Programa de Pós-Graduação em Ciências da Saúde: Medicina Tropical e Doenças Infecciosas, Belo Horizonte, Minas Gerais, Brazil.
Insights
Galectin-3 may not be a reliable biomarker for fibrosis in Chronic Chagas Cardiomyopathy (CCC). While animal studies suggest a link, human data shows no significant association, questioning its clinical utility for fibrosis assessment in Chagas disease.
Area of Science:
- Cardiology
- Immunology
- Biomarker Research
Background:
- Chronic Chagas Cardiomyopathy (CCC) is a significant cause of myocarditis, characterized by inflammation, structural changes, and fibrosis.
- Galectin-3 is implicated in inflammatory processes and myocardial fibrosis, but its role in CCC fibrosis remains unclear.
- Early identification of fibrosis intensity is crucial for guiding pharmacological therapy in CCC.
Purpose of the Study:
- To systematically review and evaluate Galectin-3 as a biomarker for fibrosis intensity in Chronic Chagas Cardiomyopathy (CCC).
Main Methods:
- A systematic review was conducted by two independent reviewers across five databases (PubMed, EMBASE, Cochrane Library, Scopus, Lilacs).
- Search terms included 'galectin-3', 'biomarkers', 'fibrosis', 'Chagas cardiomyopathy', and 'Chagas disease'.
- Seven studies (four animal models, three human) met the inclusion criteria.
Main Results:
- Experimental data from animal models (75% of studies) indicated an association between Galectin-3 expression and fibrosis in CCC.
- However, human studies (80% of studies) found no direct connection between myocardial fibrosis and Galectin-3 expression.
- Human findings did not provide significant evidence linking Galectin-3 to fibrosis development in Chagas disease.
Conclusions:
- Based on current human data, Galectin-3 may not be a suitable biomarker for assessing fibrosis intensity in Chronic Chagas Cardiomyopathy.
- Further research is needed to clarify the role of Galectin-3 in the pathophysiology of Chagas disease and its potential as a biomarker.
Abstract:
Chronic Chagas Cardiomyopathy (CCC) is the most prevalent type of myocarditis and the main clinical form of the Chagas disease, which has peculiarities such as focal inflammation, structural derangement, hypertrophy, dilation, and intense reparative fibrosis. Many cellular compounds contribute to CCC development. Galectin-3 is a partaker in inflammation and contributes to myocardial fibrosis formation. Some studies showed the connection between Galectin-3 and fibrosis in Chagas disease but are still inconclusive on the guidance for the early implementation of pharmacological therapy. This systematic review evaluated Galectin-3 as a biomarker for fibrosis intensity in CCC. Two independent reviewers have searched five databases (PubMed, EMBASE, Cochrane Library, Scopus, and Lilacs), using the following search terms: galectin-3, biomarkers, fibrosis, Chagas cardiomyopathy, and Chagas disease. Overall, seven studies met the inclusion criteria and made up this review. There were four trials conducted through animal model experiments and three trials with humans. Experimental data in mice indicate an association between Galectin-3 expression and fibrosis in CCC (75% of studies). Data from human studies showed no direct connection between myocardial fibrosis and Galectin-3 expression (80% of studies). Thus, human findings do not provide significant evidence indicating that Galectin-3 is related to fibrosis formation in Chagas disease. Based on the analyzed studies, it is suggested that Galectin-3 might not be a good fibrosis marker in CCC.
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