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Abstract
The purpose of the present study was to evaluate whether endostatin overexpression could improve cardiac function, hemodynamics, and fibrosis in heart failure (HF) via inhibiting reactive oxygen species (ROS). The HF models were established by inducing ischemia myocardial infarction (MI) through ligation of the left anterior descending (LAD) artery in Sprague–Dawley (SD) rats. Endostatin level in serum was increased in MI rats. The decrease in cardiac function and hemodynamics in MI rats were enhanced by endostatin overexpression. Endostatin overexpression inhibited the increase in collagen I, collagen III, α-smooth muscle actin (α-SMA), connective tissue growth factor (CTGF), matrix metalloproteinase (MMP)-2 and MMP9 in the hearts of MI rats. MI-induced cardiac hypertrophy was reduced by endostatin overexpression. The increased levels of malondialdehyde (MDA), superoxide anions, the promoted NAD(P)H oxidase (Nox) activity, and the reduced superoxide dismutase (SOD) activity in MI rats were reversed by endostatin overexpression. Nox4 overexpression inhibited the cardiac protective effects of endostatin. These results demonstrated that endostatin improved cardiac dysfunction and hemodynamics, and attenuated cardiac fibrosis and hypertrophy via inhibiting oxidative stress in MI-induced HF rats.
Highlights
Heart failure (HF) is showing an increasing prevalence [1]
The survival rate was reduced in myocardial infarction (MI) rats compared with the sham surgery group
The present results showed that endostatin overexpression improved cardiac function, hemodynamics, and fibrosis in the heart of MI rats; endostatin attenuated HF via inhibiting oxidative stress
Summary
The risk of HF can be elevated by myocardial infarction (MI) [2], in which cardiac remodeling occurs. Cardiac remodeling is characterized by increasing fibrosis, and accumulation of collagen type I, collagen type III, α-smooth muscle actin (α-SMA), connective tissue growth factor (CTGF), matrix metalloproteinase (MMP) 2 and MMP9 [3,4,5,6]. The expression level of endostatin in heart tissues has been reported to increase in the experimental cardiac disease models, such as MI [11,12] and pressure overload-induced cardiac hypertrophy [13,14]. Higher serum endostatin is associated with left ventricular (LV) dysfunction and an increased HF risk, but further experimental studies are needed to investigate the role of endostatin in the development of HF [15]
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