Key result
Galectin-3 fails to track myocardial fibrosis in chronic Chagas cardiomyopathy.
Why the study?
Studies linking Galectin-3 to fibrosis in Chagas disease remained inconclusive regarding guidance for the early implementation of pharmacological therapy.
Is Galectin-3 a reliable biomarker for fibrosis intensity in patients with Chronic Chagas Cardiomyopathy?
Systematic Review (n=260)
Is Galectin-3 a reliable biomarker for fibrosis intensity in patients with Chronic Chagas Cardiomyopathy?
Current evidence does not support the use of Galectin-3 as a reliable biomarker for myocardial fibrosis intensity in human Chronic Chagas Cardiomyopathy, despite positive correlations in animal models.
Evidence does not support Galectin-3 as fibrosis biomarker in human Chronic Chagas Cardiomyopathy; challenges animal model translation and warrants targeted human trials.
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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Chaves et al. (2022) conducted a systematic review in Chronic Chagas Cardiomyopathy (n=260). Galectin-3 was evaluated on Correlation between Galectin-3 expression and myocardial fibrosis intensity. Human studies do not provide significant evidence indicating that Galectin-3 is related to fibrosis formation in Chronic Chagas Cardiomyopathy, suggesting it may not be a reliable fibrosis biomarker.
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