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Bezafibrate Attenuates Pressure Overload-Induced Cardiac Hypertrophy and Fibrosis
Si-Chi Xu1, Zhen-Guo Ma1, Wen-Ying Wei1
1Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute of Wuhan University, Wuhan, China.
Insights
Bezafibrate (BZA), a PPAR-α agonist, effectively reduces cardiac hypertrophy and fibrosis caused by pressure overload. This compound shows promise in treating heart conditions linked to PPAR-α activation.
Area of Science:
- Cardiovascular Biology
- Molecular Pharmacology
Background:
- Peroxisome proliferator-activated receptor-alpha (PPAR-α) plays a role in cardiac hypertrophy.
- Bezafibrate (BZA) is a known PPAR-α agonist with potential metabolic benefits.
Purpose of the Study:
- To investigate the protective effects of Bezafibrate (BZA) against pressure overload-induced cardiac hypertrophy.
- To explore the molecular mechanisms underlying BZA's action on cardiac remodeling.
Main Methods:
- In vivo study using a mouse model of aortic banding (AB) surgery treated with BZA.
- In vitro experiments using neonatal rat ventricular cardiomyocytes (NRVMs) stimulated with phenylephrine (PE).
- Assessment of cardiac hypertrophy via echocardiography, histology, and molecular markers; evaluation of signaling pathways like AKT/GSK3β and MAPKs.
Main Results:
- BZA treatment significantly alleviated cardiac hypertrophy and fibrosis in AB-induced mice.
- BZA reduced the phosphorylation of key signaling molecules including AKT/GSK3β and MAPKs.
- In vitro, BZA suppressed PE-induced cardiomyocyte hypertrophy, an effect blocked by a PPAR-α antagonist.
Conclusions:
- Bezafibrate (BZA) demonstrates a protective effect against pressure overload-induced cardiac hypertrophy and fibrosis.
- The findings suggest that BZA's therapeutic potential in cardiac remodeling is mediated through PPAR-α activation.
Abstract:
Background. Peroxisome proliferator-activated receptor-α (PPAR-α) is closely associated with the development of cardiac hypertrophy. Previous studies have indicated that bezafibrate (BZA), a PPAR-α agonist, could attenuate insulin resistance and obesity. This study was designed to determine whether BZA could protect against pressure overload-induced cardiac hypertrophy. Methods. Mice were orally given BZA (100 mg/kg) for 7 weeks beginning 1 week after aortic banding (AB) surgery. Cardiac hypertrophy was assessed based on echocardiographic, histological, and molecular aspects. Moreover, neonatal rat ventricular cardiomyocytes (NRVMs) were used to investigate the effects of BZA on the cardiomyocyte hypertrophic response in vitro. Results. Our study demonstrated that BZA could alleviate cardiac hypertrophy and fibrosis in mice subjected to AB surgery. BZA treatment also reduced the phosphorylation of protein kinase B (AKT)/glycogen synthase kinase-3β (GSK3β) and mitogen-activated protein kinases (MAPKs). BZA suppressed phenylephrine- (PE-) induced hypertrophy of cardiomyocyte in vitro. The protective effects of BZA were abolished by the treatment of the PPAR-α antagonist in vitro. Conclusions. BZA could attenuate pressure overload-induced cardiac hypertrophy and fibrosis.
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