Chlorogenic acid, an ester of caffeic acid and quinic acid, is found in foods such as eggplant and peaches. Its role in heart disease remains poorly understood. This study investigated whether chlorogenic acid affects cardiac hypertrophy and fibrosis in animal and cellular models of isoproterenol-induced cardiac hypertrophy. Treatment of isoproterenol-stimulated cardiomyocytes with chlorogenic acid reduced cell size and the expression levels of cardiac hypertrophy-related genes. In the animal model, isoproterenol was delivered via an osmotic minipump for 2 weeks to induce cardiac hypertrophy, and chlorogenic acid was intraperitoneally administered for the same duration. Echocardiographic analysis showed that chlorogenic acid significantly reduced wall thickness in mice. Picrosirius red staining, quantitative reverse transcription polymerase chain reaction, and Western blot analysis revealed that cardiac fibrosis was attenuated by chlorogenic acid. Chlorogenic acid treatment downregulated galectin 3 (Lgals3), a fibrosis-associated gene that had been upregulated by isoproterenol stimulation. Galectin 3 knockdown ameliorated isoproterenol-induced cardiac hypertrophy and reduced the expression levels of COL1A1 and ADAMTS8; galectin 3 overexpression increased cardiomyocyte size and upregulated COL1A1 and ADAMTS8 expression levels. These findings suggest that chlorogenic acid could serve as a novel treatment for cardiac hypertrophy and fibrosis via downregulation of galectin 3.