Aim To investigate the role of galectin-3 (Gal-3) in ventricular remodeling of heart insufficiency, via the pathway of Gal-3 specific competitive antagonist--modified citrus pectin (MCP) inhibiting Gal-3. Methods 30 rabbits were randomly divided into sham operation group, cardiac insufficiency group and MCP group. A model of cardiac dysfunction after myocardial infarction was made by ligating the anterior descending branch of coronary artery. After the model was successfully made, MCP group was treated with 75 g/L MCP allocated with normal saline, and intragastric administration for 4 weeks with 2 mL/(kg·d), and sham operation group and cardiac insufficiency group received the intragastric administration of 2 mL/(kg·d) normal saline for 4 weeks. Before operation and 2,4, 6 weeks after operation, cardiac function was measured by cardiac ultrasound, and serum levels of Gal-3 and brain natriuretic peptide (BNP) were detected by ELISA. The mRNA expressions of Gal-3, collagen Ⅰ and Ⅲ in myocardial tissue were detected by real-time quantitative PCR, and the ratio of Ⅰ/Ⅲ was calculated. 6 weeks after operation, Masson staining was used to observe the histopathology of myocardial infarction region, and the protein expressions of Gal-3, collagen Ⅰ and Ⅲ were detected by Western blot. Results After 4 weeks of administration, the heart function of the MCP group was significantly improved compared with the cardiac insufficiency group (P＜0.01). The serum Gal-3 in cardiac insufficiency group was higher than that in sham operation group (P＜0.05), and serum Gal-3 in MCP group was significantly lower than that in cardiac insufficiency group (P＜0.05). Correlation analysis showed that left ventricular ejection fraction was negatively correlated with serum Gal-3 (r＝－0.841, P＝0.009), and left ventricular end-diastolic diameter was positively correlated with serum Gal-3 (r＝0.905, P＝0.002), in cardiac insufficiency group. Compared with cardiac insufficiency group, the mRNA expression of Gal-3, collagen Ⅰ and Ⅲ in MCP group was significantly decreased (P＜0.05). Under optical microscope, cardiac insufficiency group showed myocardial cell disorder, part of myocardial cell necrosis, edema, acollagen deposition and inflammatory cell infiltration; MCP group showed myocardial fiber thickening, arranging in a slightly tidy order. Protein expressions of Gal-3, collagen Ⅰ and Ⅲ in the infarcted myocardium of cardiac insufficiency group were significantly higher than those in MCP group and sham operation group. Correlation analysis showed that Gal-3 in infarction region was positively correlated with collagen Ⅲ in cardiac insufficiency group (r＝0.793, P＝0.019). Conclusion Gal-3 plays a key role in the progressions of ventricular remodeling and myocardial fibrosis in heart failure.