Abstract
SIRT1 (silent information regulator 1) is a histone deacetylase. It can sense the energy level in cells and delay cell senescence, leading to resistance to external stress and improving metabolism. Mitral regurgitation (MR) is a common disease in cardiac surgery. However, there are no previous studies on SIRT1 and left atrial fibrosis caused by MR. In this study, we aimed to explore the regulatory effect of SIRT1 on left atrial fibrosis induced by MR. We used Guizhou miniature pigs to establish an MR model and a sham operation model after anaesthesia induction and respiratory intubation, and these model animals were followed for 30 months after the surgery. The differential distribution and expression of SIRT1 and collagen I in the left atrium was determined by immunofluorescence and Western blotting. Furthermore, we treated NIH3T3 fibroblasts (CFs) with resveratrol and Angiotensin II (Ang II) to analyse the specific mechanism involved in the development of myocardial fibrosis. The results showed that the MR model was successfully constructed. There were 8 pigs in the MR group and 6 pigs in the control group. In both the animal experiments and the cell experiments, the expression of collagen I in the MR group was increased significantly compared to that in the control group, while the expression of SIRT1 was decreased.
Highlights
Atrial remodelling (AR) refers to a series of changes in size, including shape, wall thickness and tissue structure, due to increased or damaged load of the atrium
We aimed to explore the regulatory effect of SIRT1 on left atrial fibrosis induced by mitral regurgitation (MR)
Compared with that of the left atrium, the collagen volume fraction (CVF) of the left ventricle in the model group was 2.0 ± 0.5% and was 1.9 ± 0.3% in the control group, and there was no significant difference between the two groups (P = 0.58) (Fig. 1B)
Summary
Atrial remodelling (AR) refers to a series of changes in size, including shape, wall thickness and tissue structure, due to increased or damaged load of the atrium. This pathophysiological process involves lesion repair and compensation of the atrium[1,2,3]. Since small animals are prone to heart failure and www.nature.com/scientificreports cardiac dysfunction after modelling, long-term feeding is difficult; there is a lack of long-term observational studies on SIRT1 and myocardial fibrosis simulating the clinical disease process. To preliminarily explore the role of SIRT1 in left atrial remodeling and myocardial fibrosis, this experiment aimed to establish a mitral regurgitation (MR) model in miniature pigs and carried out long-term observations on the regulatory role of SIRT1 in mitral regurgitation-induced left atrial fibrosis
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