Abstract
The transverse aortic constriction (TAC) model surgery is a widely used disease model to study pressure overload–induced cardiac hypertrophy and heart failure in mice. The severity of adverse cardiac remodeling of the TAC model is largely dependent on the degree of constriction around the aorta, and the phenotypes of TAC are also different in different mouse strains. Few studies focus on directly comparing phenotypes of the TAC model with different degrees of constriction around the aorta, and no study compares the difference in C57BL/6N mice. In the present study, C57BL/6N mice aged 10 weeks were subjected to sham, 25G TAC, 26G TAC, and 27G TAC surgery for 4 weeks. We then analyzed the different phenotypes induced by 25G TAC, 26G TAC, and 27G TAC in c57BL/6N mice in terms of pressure gradient, cardiac hypertrophy, cardiac function, heart failure situation, survival condition, and cardiac fibrosis. All C57BL/6N mice subjected to TAC surgery developed significantly hypertrophy. Mice subjected to 27G TAC had severe cardiac dysfunction, severe cardiac fibrosis, and exhibited characteristics of heart failure at 4 weeks post-TAC. Compared with 27G TAC mice, 26G TAC mice showed a much milder response in cardiac dysfunction and cardiac fibrosis compared to 27G TAC, and a very small fraction of the 26G TAC group exhibited characteristics of heart failure. There was no obvious cardiac dysfunction, cardiac fibrosis, and characteristics of heart failure observed in 25G TAC mice. Based on our results, we conclude that the 25G TAC, 26G TAC, and 27G TAC induced distinct phenotypes in C57BL/6N mice.
Highlights
Heart failure (HF) is still one of the leading causes of mortality worldwide, and the prevalence of HF continues to rise over time
There was no statistically significant difference between 25 and 26 G transverse aortic constriction (TAC), the pressure gradient in 26 G TAC was much higher than that in 25 G TAC. These results show that the different needle sizes have successfully induced different degrees of pressure overload conditions in C57BL/6N mice
All C57BL/6N mice subjected to TAC surgery developed significant hypertrophy
Summary
Heart failure (HF) is still one of the leading causes of mortality worldwide, and the prevalence of HF continues to rise over time. It is more important to better understand the development of HF and find new therapeutic targets. The development of HF is characterized by a process of adverse cardiac remodeling [2], and there. Distinct TAC Phenotypes in C57BL6/N are three major patterns of cardiac remodeling: pressure overload–induced concentric hypertrophy, volume overload– induced eccentric hypertrophy, and mixed load–induced postmyocardial-infarct remodeling [3]. Heart disease animal models play an important role in studying these remodeling processes as well as in preclinical studies. The validity and accuracy of animal models are necessary for the mechanism study of HF and for new drug development as well [4, 5]
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