Abstract
Objection: Cumulative studies have identified the effectiveness of cardiac shock wave therapy (CSWT) in treating heart failure after acute myocardial infarction (AMI), but little have been discussed with regard to the beneficial effects of CSWT on anti-fibrosis along with the underlying mechanism. In this study, we investigated whether CSWT could reduce post-AMI fibrosis and further explored the molecular mechanism.Methods: Rat heart failure (HF) models induced by ligating the left anterior descending coronary artery were established and validated by echocardiography. Eligible animals were randomly categorized into five groups: the sham group, the HF group, the HF + CSWT group, the HF + LY294002 group, and the HF + CSWT + LY294002 group. The cardiac weight, serum level of BNP, NT-pro BNP and echocardiography parameters were measured to assess cardiac function in different groups. Masson's trichrome staining was used to assess the proportions of the fibrotic area. The expression level of CD34, αSMA was measured by RT-PCR, Immunohistochemistry and Immunofluorescent analyses and the level of PI3K/Akt was quantified by Immunohistochemistry and Western blotting.Results: The application of CSWT significantly improved cardiac function and reduced myocardial fibrosis and level of CD34 and αSMA, compared to the HF group. CSWT led to significant elevations of p-PI3K and p-Akt expression levels compared to that of the HF group and the inhibition of the PI3K/Akt pathway abolished the observed beneficial effects of CSWT.Conclusion: CSWT can facilitate the alleviation of cardiac fibrosis induced by AMI through the activation of PI3K/Akt signaling pathway.
Highlights
MATERIALS AND METHODSAccounting for a staggering 30% of all deaths, ischemia heart disease (IHD) is the primary cause of global mortality and has long been considered as a life-threatening problem [1]
The inhibition of fibrosis is gaining increasing attention for the reason that if effective anti-fibrosis can be achieved in infarcted myocardium and the border region, the pathophysiologic process of ventricular remodeling leading to heart failure (HF) may be restrained, and the prognosis of HF patients could be substantially improved
Based on previous results that cardiac shock wave therapy (CSWT) benefited cardiac function and alleviated myocardium fibrosis, we examined whether PI3K/Akt signaling pathway, a key factor that has been shown to be responsible for withholding fibrotic progression after acute myocardial infarction (AMI), involved in the process of anti-fibrosis
Summary
MATERIALS AND METHODSAccounting for a staggering 30% of all deaths, ischemia heart disease (IHD) is the primary cause of global mortality and has long been considered as a life-threatening problem [1]. The loss of normal cardiomyocytes initiated by myocardium infarction can eventually triggers the replacement of necrotic zone by fibrous scar tissue, which generally has invalid systolic function. This is known as ventricular remodeling and can result in post-infarction heart failure (HF). The inhibition of fibrosis is gaining increasing attention for the reason that if effective anti-fibrosis can be achieved in infarcted myocardium and the border region, the pathophysiologic process of ventricular remodeling leading to HF may be restrained, and the prognosis of HF patients could be substantially improved.
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