Perindopril and a Galectin-3 Inhibitor Improve Ischemic Heart Failure in Rabbits by Reducing Gal-3 Expression and Myocardial Fibrosis

Li, Sha; Li, Shuren; Hao, Xiaoyan; Zhang, Yuehua; Deng, Wenhao

doi:10.3389/fphys.2019.00267

Cited by 31 publications

(29 citation statements)

References 32 publications

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“… 25 , 26 Additionally, a Gal-3 inhibitor alleviated collagen deposition and significantly decreased fibrosis. 14 In our study, CTGF and Gla-3 protein levels were suppressed by CCM in rabbits with CHF, which may be a potential mechanism by which CCM attenuated structural remodeling.…”

Section: Discussionsupporting

confidence: 57%

Cardiac contractility modulation attenuates structural and electrical remodeling in a chronic heart failure rabbit model

et al. 2020

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Background Cardiac contractility modulation (CCM) is non-excitatory electrical stimulation for improving cardiac function. This study aimed to evaluate the effects of CCM on structural and electrical remodeling in a rabbit model of chronic heart failure (CHF). Methods Thirty rabbits were randomly divided into the sham, CHF, and CCM groups. The CHF model was induced 12 weeks after trans-aortic constriction by pressure unloading and CCM was delivered to the myocardium for 4 weeks. Corrected QT intervals, the ventricular effective refractory period, and inducibility of ventricular tachycardia were measured by an electrophysiological examination. Connective tissue growth factor, galectin-3, Kv4.3, KCNQ1, KCNH2, and connexin 43 protein levels were measured by western blotting. Results The CHF group had a significantly prolonged corrected QT interval and ventricular effective refractory period, and increased inducibility of ventricular tachycardia. Prominent myocardial fibrosis and increased hydroxyproline content were observed in the CHF group, but these were suppressed in the CCM group. Kv4.3, KCNQ1, KCNH2, and connexin 43 protein levels were significantly lower in the CHF group, but treatment with CCM partially restored their levels. Conclusions CCM attenuates myocardial structural and electrical remodeling during CHF. These findings provide evidence for clinical use of CCM in treating CHF.

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Section: Discussionsupporting

confidence: 57%

Cardiac contractility modulation attenuates structural and electrical remodeling in a chronic heart failure rabbit model

et al. 2020

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“…It has been demonstrated that overexpressing CTGF induce cardiac hypertrophy and collagen production and CTGF is a well-characterized downstream mediator of TGF-β1/Smad3 signaling pathway during the fibrotic response [21,22]. Anther study shown the galectin-3 inhibitor alleviated collagen deposition and significantly decreased fibrosis [10]. In our study, the protein level of CTGF, Gla-3 were suppressed with CCM therapy in CHF rabbits.…”

Section: Effect Of Ccm Treatment On Structural Remolding In Heart Faisupporting

confidence: 55%

“…It has been demonstrated that connective tissue growth factor (CTGF) and galectin-3 (Gal-3) are novel pro-fibrotic markers. Those bio-makers are involved in physiological conditions, such as promoting fibroblast proliferation and collagen deposition, thus lead to myocardial structural remolding [9,10]. In addition to alterations in Connexin43 (Cx43) expression, changes in potassium currents are important contributors to myocardial electrical remodeling [11,12].…”

Section: Introductionmentioning

confidence: 99%

Cardiac contractility modulation regulates the structural and electrical remolding in chronic heart failure rabbit model

Zhang

Dang

Hao

et al. 2019

Preprint

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Background Chronic heart failure (CHF) is accompanied by complex changes in cardiac electrophysiology and functional properties of cardiomyocytes which cause the structural and electrical remodeling process. Cardiac contractility modulation (CCM) is a novel therapeutic method and has proven to be effective in improving cardiac function. This study evaluated the effects of CCM on structural and electrical remolding in a rabbit model of CHF. Methods Thirty rabbits were randomly divided into sham group, heart failure group and CCM group. CHF model was induced 12 weeks after trans aortic constriction by pressure unloading. Then cardiac contractility modulation was delivered to the myocardium lasting six hours per day for 4 weeks. Structural changes were assessed by hydroxyproline assay and picrosirius red staining. The QTc intervals, ventricular effective refractory period and the inducibility of ventricular tachycardia were measured by electrophysiological examination. Protein levels of CTGF, Gal-3, Kv4.3, KCNQ1, KCNH2 and CX43 were measured by western blot analysis. Results Our study revealed that CHF rabbits developed significant prolonged QTc, ventricular effective refractory period and increased inducibility of ventricular tachycardia. Prominent myocardial fibrosis and increased levels of hydroxyproline content were observed in the heart failure group. Changes mentioned above can be suppressed with CCM therapy in CHF rabbits. The protein levels of CTGF, Gal-3, Kv4.3, KCNQ1, KCNH2 and CX43 significantly increased in the heart failure group, but these changes were prevented in the CCM group. Conclusions The present study demonstrated that CCM treatment prevented myocardial structural and electrical remolding in a rabbit model of CHF. The beneficial effect of CCM may be related to prevention of downregulation of the CTGF, Gal-3, Kv4.3, KCNQ1, KCNH2 and CX43. These findings provide experimental evidence for the clinical use of CCM in the treatment of HF.

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“…It was suggested that microvascular dysfunction is one of the major processes in the development of ischemic heart failure [12]. The endothelium of coronary vessels could regulate coronary blood flow in epicardial coronary and intramyocardial microcirculations [13].…”

Section: Discussionmentioning

confidence: 99%

The Effect of YiQiFuMai on Ischemic Heart Failure by Improve Myocardial Microcirculation and Increase eNOS and VEGF Expression

Li¹,

Hao²,

Xiao³

et al. 2020

IJCM

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Objective: To assess the effects of traditional Chinese medicine YiQiFuMai on cardiac function during the progression of ischemic heart failure. Methods: Rabbits were divided into sham, heart failure, and YiQiFuMai groups. The ischemic heart failure model was established in New Zealand white rabbits, which were intraperitoneally injected with YiQiFuMai injection and 0.9% sodium chloride after the operation. After six weeks, cardiac function was examined by ultrasound; serum BNP levels were measured by ELISA; p-AKT, eNOS, ICAM-1 and VEGF levels were evaluated by real-time PCR and Western-Blot; pathological changes of the myocardial tissue were observed by H&E staining; CD31 expression in tissue samples was analyzed by immunohistochemistry. The ultrastructure and microcirculation of myocardial tissue specimens from the three groups were assessed by transmission electron microscopy. Results: YiQiFuMai decreased serum BNP levels, and increased LVEF and reduced LVEDD at 6 weeks postoperatively. In addition, YiQiFuMai can improve myocardial damage and microcirculation structure, as assessed by histology and transmission electron microscope. At the molecular level, treatment with YiQiFuMai resulted in increased eNOS, VEGF and p-AKT levels but reduced ICAM-1 amounts compared with the heart failure group. Conclusion: Ischemic heart failure damages the microvascular structure and functions of the myocardium. Treatment with YiQiFuMai potentially ameliorates microcirculatory damage and alleviates cardiac failure by improving endothelial function and angiogenesis, and inhibiting inflammatory cell adhesion.

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Perindopril and a Galectin-3 Inhibitor Improve Ischemic Heart Failure in Rabbits by Reducing Gal-3 Expression and Myocardial Fibrosis

Cited by 31 publications

References 32 publications

Cardiac contractility modulation attenuates structural and electrical remodeling in a chronic heart failure rabbit model

Cardiac contractility modulation attenuates structural and electrical remodeling in a chronic heart failure rabbit model

Cardiac contractility modulation regulates the structural and electrical remolding in chronic heart failure rabbit model

The Effect of YiQiFuMai on Ischemic Heart Failure by Improve Myocardial Microcirculation and Increase eNOS and VEGF Expression

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