Chlorogenic acid attenuates cardiac hypertrophy and fibrosis by downregulating galectin 3
Abstract 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 isoprot...
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Nature Portfolio
2025-07-01
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| Online Access: | https://doi.org/10.1038/s41598-025-12222-0 |
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| author | Seong Hoon Kim Hae Jin Kee Hongyan Zhou Hyukjin Park Seung Hun Lee Doo Sun Sim Myung Ho Jeong Young Joon Hong |
| author_facet | Seong Hoon Kim Hae Jin Kee Hongyan Zhou Hyukjin Park Seung Hun Lee Doo Sun Sim Myung Ho Jeong Young Joon Hong |
| author_sort | Seong Hoon Kim |
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| description | Abstract 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. |
| format | Article |
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| institution | Kabale University |
| issn | 2045-2322 |
| language | English |
| publishDate | 2025-07-01 |
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| spelling | doaj-art-dface581f81b44b081473c5b41924f242025-08-20T03:42:49ZengNature PortfolioScientific Reports2045-23222025-07-0115111610.1038/s41598-025-12222-0Chlorogenic acid attenuates cardiac hypertrophy and fibrosis by downregulating galectin 3Seong Hoon Kim0Hae Jin Kee1Hongyan Zhou2Hyukjin Park3Seung Hun Lee4Doo Sun Sim5Myung Ho Jeong6Young Joon Hong7Department of Cardiology, Chonnam National University Medical SchoolHeart Research Center of Chonnam National University HospitalDepartment of Cardiology, Chonnam National University Medical SchoolDepartment of Cardiology, Chonnam National University Medical SchoolDepartment of Cardiology, Chonnam National University Medical SchoolDepartment of Cardiology, Chonnam National University Medical SchoolDepartment of Cardiology, Chonnam National University Medical SchoolDepartment of Cardiology, Chonnam National University Medical SchoolAbstract 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.https://doi.org/10.1038/s41598-025-12222-0Chlorogenic acidGalectin 3Cardiac hypertrophyFibrosisA disintegrin and metalloproteinase with thrombospondin motifs 8 |
| spellingShingle | Seong Hoon Kim Hae Jin Kee Hongyan Zhou Hyukjin Park Seung Hun Lee Doo Sun Sim Myung Ho Jeong Young Joon Hong Chlorogenic acid attenuates cardiac hypertrophy and fibrosis by downregulating galectin 3 Scientific Reports Chlorogenic acid Galectin 3 Cardiac hypertrophy Fibrosis A disintegrin and metalloproteinase with thrombospondin motifs 8 |
| title | Chlorogenic acid attenuates cardiac hypertrophy and fibrosis by downregulating galectin 3 |
| title_full | Chlorogenic acid attenuates cardiac hypertrophy and fibrosis by downregulating galectin 3 |
| title_fullStr | Chlorogenic acid attenuates cardiac hypertrophy and fibrosis by downregulating galectin 3 |
| title_full_unstemmed | Chlorogenic acid attenuates cardiac hypertrophy and fibrosis by downregulating galectin 3 |
| title_short | Chlorogenic acid attenuates cardiac hypertrophy and fibrosis by downregulating galectin 3 |
| title_sort | chlorogenic acid attenuates cardiac hypertrophy and fibrosis by downregulating galectin 3 |
| topic | Chlorogenic acid Galectin 3 Cardiac hypertrophy Fibrosis A disintegrin and metalloproteinase with thrombospondin motifs 8 |
| url | https://doi.org/10.1038/s41598-025-12222-0 |
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