Alleviation of fibrosis and oxidative stress in pressure overload-induced cardiac remodeling and heart failure via SIRT3 activation by colchicine

Heart failure (HF) is the end stage of many cardiovascular diseases, which is often associated with myocardial hypertrophy and cardiac remodeling. Among them, pressure overload-induced myocardial injury is one of the most common causes of heart failure. Colchicine, a drug widely used in the treatmen...

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Vydáno v:	Biochemical and biophysical research communications Ročník 770; s. 151957
Hlavní autoři:	Wu, Mengze, Chen, Guodong, Peng, Yuce, Luo, Suxin
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States Elsevier Inc 12.07.2025
Témata:	agonists Animals atrial fibrillation Colchicine Colchicine - pharmacology Colchicine - therapeutic use coronary artery disease drugs fibroblasts Fibroblasts - drug effects Fibroblasts - metabolism Fibroblasts - pathology Fibrosis Heart failure Heart Failure - drug therapy Heart Failure - metabolism Heart Failure - pathology hypertrophy Male Mice Mice, Inbred C57BL Myocardium - metabolism Myocardium - pathology Oxidative stress Oxidative Stress - drug effects risk reduction simulation models SIRT3 Sirtuin 3 - metabolism therapeutics Ventricular Remodeling - drug effects Heart failure Oxidative stress Colchicine Fibrosis SIRT3
ISSN:	0006-291X, 1090-2104, 1090-2104
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Abstract	Heart failure (HF) is the end stage of many cardiovascular diseases, which is often associated with myocardial hypertrophy and cardiac remodeling. Among them, pressure overload-induced myocardial injury is one of the most common causes of heart failure. Colchicine, a drug widely used in the treatment of inflammatory diseases, has recently been found to significantly reduce the risk of cardiovascular events in patients with coronary artery disease and atrial fibrillation. However, the specific mechanism of colchicine has not been fully elucidated. We used the transverse aortic constriction (TAC) model to simulate cardiac pressure overload in mice. We found that colchicine attenuated TAC-induced heart failure and alleviated cardiac oxidative stress and fibrosis. To explore the specific molecular mechanism, we treated primary cardiac fibroblasts (CFs) and HL-1 with Ang Ⅱ in vitro to simulate the occurrence of TAC model. We found that colchicine induced SIRT3 activation and alleviated myocardial oxidative stress and cadiac fibrosis. Additionally, the SIRT3-selective agonist HKL exerts similar effects to colchicine, whereas the SIRT3-selective inhibitor 3-TYP partially reverses the therapeutic effects of colchicine. Our findings suggest that colchicine reduced cardiac oxidative stress and fibrosis by activating SIRT3, which in turn alleviated the progression of pressure overload-induced heart failure. Fig. 7. Graphical AbstractColchicine ameliorates TAC-induced myocardial injury and heart failure by activating SIRT3, which subsequently activates the NRF2/NQO1 antioxidant pathway and inhibits the α-SMA/TGF-β fibrotic pathway. Created in BioRender. Zhang, L. (2025) https://BioRender.com/ji7p2oo. [Display omitted] •Colchicine alleviates pressure overload-induced cardiac remodeling and heart failure.•Colchicine alleviates pressure overload-induced cardiac fibrosis.•Colchicine reduces pressure overload-induced myocardial oxidative stress.•Colchicine exerts a cardioprotective effect by activating SIRT3 pathway.
AbstractList	Heart failure (HF) is the end stage of many cardiovascular diseases, which is often associated with myocardial hypertrophy and cardiac remodeling. Among them, pressure overload-induced myocardial injury is one of the most common causes of heart failure. Colchicine, a drug widely used in the treatment of inflammatory diseases, has recently been found to significantly reduce the risk of cardiovascular events in patients with coronary artery disease and atrial fibrillation. However, the specific mechanism of colchicine has not been fully elucidated. We used the transverse aortic constriction (TAC) model to simulate cardiac pressure overload in mice. We found that colchicine attenuated TAC-induced heart failure and alleviated cardiac oxidative stress and fibrosis. To explore the specific molecular mechanism, we treated primary cardiac fibroblasts (CFs) and HL-1 with Ang Ⅱ in vitro to simulate the occurrence of TAC model. We found that colchicine induced SIRT3 activation and alleviated myocardial oxidative stress and cadiac fibrosis. Additionally, the SIRT3-selective agonist HKL exerts similar effects to colchicine, whereas the SIRT3-selective inhibitor 3-TYP partially reverses the therapeutic effects of colchicine. Our findings suggest that colchicine reduced cardiac oxidative stress and fibrosis by activating SIRT3, which in turn alleviated the progression of pressure overload-induced heart failure. Heart failure (HF) is the end stage of many cardiovascular diseases, which is often associated with myocardial hypertrophy and cardiac remodeling. Among them, pressure overload-induced myocardial injury is one of the most common causes of heart failure. Colchicine, a drug widely used in the treatment of inflammatory diseases, has recently been found to significantly reduce the risk of cardiovascular events in patients with coronary artery disease and atrial fibrillation. However, the specific mechanism of colchicine has not been fully elucidated. We used the transverse aortic constriction (TAC) model to simulate cardiac pressure overload in mice. We found that colchicine attenuated TAC-induced heart failure and alleviated cardiac oxidative stress and fibrosis. To explore the specific molecular mechanism, we treated primary cardiac fibroblasts (CFs) and HL-1 with Ang Ⅱ in vitro to simulate the occurrence of TAC model. We found that colchicine induced SIRT3 activation and alleviated myocardial oxidative stress and cadiac fibrosis. Additionally, the SIRT3-selective agonist HKL exerts similar effects to colchicine, whereas the SIRT3-selective inhibitor 3-TYP partially reverses the therapeutic effects of colchicine. Our findings suggest that colchicine reduced cardiac oxidative stress and fibrosis by activating SIRT3, which in turn alleviated the progression of pressure overload-induced heart failure.Heart failure (HF) is the end stage of many cardiovascular diseases, which is often associated with myocardial hypertrophy and cardiac remodeling. Among them, pressure overload-induced myocardial injury is one of the most common causes of heart failure. Colchicine, a drug widely used in the treatment of inflammatory diseases, has recently been found to significantly reduce the risk of cardiovascular events in patients with coronary artery disease and atrial fibrillation. However, the specific mechanism of colchicine has not been fully elucidated. We used the transverse aortic constriction (TAC) model to simulate cardiac pressure overload in mice. We found that colchicine attenuated TAC-induced heart failure and alleviated cardiac oxidative stress and fibrosis. To explore the specific molecular mechanism, we treated primary cardiac fibroblasts (CFs) and HL-1 with Ang Ⅱ in vitro to simulate the occurrence of TAC model. We found that colchicine induced SIRT3 activation and alleviated myocardial oxidative stress and cadiac fibrosis. Additionally, the SIRT3-selective agonist HKL exerts similar effects to colchicine, whereas the SIRT3-selective inhibitor 3-TYP partially reverses the therapeutic effects of colchicine. Our findings suggest that colchicine reduced cardiac oxidative stress and fibrosis by activating SIRT3, which in turn alleviated the progression of pressure overload-induced heart failure. Heart failure (HF) is the end stage of many cardiovascular diseases, which is often associated with myocardial hypertrophy and cardiac remodeling. Among them, pressure overload-induced myocardial injury is one of the most common causes of heart failure. Colchicine, a drug widely used in the treatment of inflammatory diseases, has recently been found to significantly reduce the risk of cardiovascular events in patients with coronary artery disease and atrial fibrillation. However, the specific mechanism of colchicine has not been fully elucidated. We used the transverse aortic constriction (TAC) model to simulate cardiac pressure overload in mice. We found that colchicine attenuated TAC-induced heart failure and alleviated cardiac oxidative stress and fibrosis. To explore the specific molecular mechanism, we treated primary cardiac fibroblasts (CFs) and HL-1 with Ang Ⅱ in vitro to simulate the occurrence of TAC model. We found that colchicine induced SIRT3 activation and alleviated myocardial oxidative stress and cadiac fibrosis. Additionally, the SIRT3-selective agonist HKL exerts similar effects to colchicine, whereas the SIRT3-selective inhibitor 3-TYP partially reverses the therapeutic effects of colchicine. Our findings suggest that colchicine reduced cardiac oxidative stress and fibrosis by activating SIRT3, which in turn alleviated the progression of pressure overload-induced heart failure. Fig. 7. Graphical AbstractColchicine ameliorates TAC-induced myocardial injury and heart failure by activating SIRT3, which subsequently activates the NRF2/NQO1 antioxidant pathway and inhibits the α-SMA/TGF-β fibrotic pathway. Created in BioRender. Zhang, L. (2025) https://BioRender.com/ji7p2oo. [Display omitted] •Colchicine alleviates pressure overload-induced cardiac remodeling and heart failure.•Colchicine alleviates pressure overload-induced cardiac fibrosis.•Colchicine reduces pressure overload-induced myocardial oxidative stress.•Colchicine exerts a cardioprotective effect by activating SIRT3 pathway.
ArticleNumber	151957
Author	Peng, Yuce Wu, Mengze Luo, Suxin Chen, Guodong
Author_xml	– sequence: 1 givenname: Mengze surname: Wu fullname: Wu, Mengze – sequence: 2 givenname: Guodong surname: Chen fullname: Chen, Guodong – sequence: 3 givenname: Yuce surname: Peng fullname: Peng, Yuce email: China.pyc@live.com – sequence: 4 givenname: Suxin surname: Luo fullname: Luo, Suxin email: luosuxin@hospital.cqmu.edu.cn
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CitedBy_id	crossref_primary_10_1016_j_phrs_2025_107936
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Keywords	Heart failure Oxidative stress Colchicine Fibrosis SIRT3
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Snippet	Heart failure (HF) is the end stage of many cardiovascular diseases, which is often associated with myocardial hypertrophy and cardiac remodeling. Among them,...
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SubjectTerms	agonists Animals atrial fibrillation Colchicine Colchicine - pharmacology Colchicine - therapeutic use coronary artery disease drugs fibroblasts Fibroblasts - drug effects Fibroblasts - metabolism Fibroblasts - pathology Fibrosis Heart failure Heart Failure - drug therapy Heart Failure - metabolism Heart Failure - pathology hypertrophy Male Mice Mice, Inbred C57BL Myocardium - metabolism Myocardium - pathology Oxidative stress Oxidative Stress - drug effects risk reduction simulation models SIRT3 Sirtuin 3 - metabolism therapeutics Ventricular Remodeling - drug effects
Title	Alleviation of fibrosis and oxidative stress in pressure overload-induced cardiac remodeling and heart failure via SIRT3 activation by colchicine
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