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Updated: May 10, 2026
A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats
Published on: December 2, 2016
[Autophagic flux of cardiomyocytes from 20-week transverse abdominal aortic constriction rats]
Long-Biao Cui1, Juan-Juan Sheng, Yun-Ying Wang
1Key Laboratory of Aerospace Medicine, Ministry of Education, Department of Aerospace Physiology, the Fourth Military Medical University, Xi'an 710032, China.
Insights
Cardiac autophagy flux remains unchanged in rats with sustained pressure overload-induced heart failure. This suggests a balance between hypertrophy inhibition and pressure load stress on autophagy during heart remodeling.
Area of Science:
- Cardiovascular Biology
- Cellular Biology
- Autophagy Research
Background:
- Cardiac autophagy increases in heart failure due to pressure overload.
- The role of enhanced autophagy in myocardial protection or heart failure progression is unclear.
Purpose of the Study:
- To investigate autophagic flux in cardiomyocytes of rats with sustained pressure overload-induced cardiac hypertrophy.
- To determine if autophagy plays a protective or detrimental role in the transition to heart failure.
Main Methods:
- Transverse abdominal aortic constriction (TAC) in rats for 20 weeks to induce cardiac hypertrophy.
- Echocardiography to assess cardiac structure and function.
- Immunofluorescent histochemistry and Western blot to analyze autophagic flux markers (LC3, cathepsin D, ubiquitin, p62).
- Fasting rats as a positive control for cardiac autophagy.
Main Results:
- Fasting (3 days) augmented autophagic flux in cardiomyocytes, indicated by increased LC3 and cathepsin D staining.
- 20-week TAC rats showed no significant changes in autophagic markers (LC3, cathepsin D, ubiquitin, p62) compared to sham rats.
- Cardiac structure and function parameters were altered by fasting but not significantly changed in TAC rats regarding autophagic markers.
Conclusions:
- Autophagic flux in cardiomyocytes is unchanged in the middle to late stages of cardiac hypertrophy induced by sustained pressure overload.
- This suggests a compensatory balance between the inhibitory effects on hypertrophy and the activating effects of pressure load stress on autophagy.
- Further research is needed to elucidate the precise role of autophagy in pressure overload-induced heart failure progression.
Abstract:
Cardiac autophagy dramatically increases in heart failure induced by sustained pressure overload. However, it has not yet been addressed if enhanced autophagy plays a role in protecting myocardium or mediating progression from compensative hypertrophy to heart failure. The aim of the present study was to detect autophagic flux of cardiomyocytes from 20-week transverse abdominal aortic constriction (TAC) rats. Fasting rats were used as the positive control for detecting cardiac autophagy. Echocardiography was applied to find the changes of cardiac structure and function. Immunofluorescent histochemistry and Western blot were used to analyze the related biomolecular indexes reflecting cardiac autophagic flux. After the previous methods for detecting cardiac autophagy were confirmed, the autophagic flux in cardiomyocytes of rats subjected to 20-week TAC was examined. The results showed that fasting had no obvious influence on parameters of cardiac structure in rats, including interventricular septal wall thickness and left ventricle posterior wall thickness, but heart rate, diastolic left ventricle internal dimension, fractional shortening of left ventricle dimension, ejection fraction and mitral inflow velocity decreased in rats after fasting for 3 d. Meanwhile, positively stained particles of LC3 and cathepsin D, but not ubiquitin and complement 9, distributed within cardiomyocytes of 3-day fasting rats, indicating augmented autophagic flux. Compared with sham rats, 20-week TAC rats did not show any changes of LC3, cathepsin D, ubiquitin and complement 9 in myocardium detected by immunofluorescent histochemistry. In addition, protein levels of LC3, cathepsin D and p62 in myocardium of TAC rats did not changed. These results reveal the unchanged autophagic flux in cardiomyocytes at middle or late phase of cardiac hypertrophy in TAC rats, implying a balance between inhibition of hypertrophy and activation of pressure load stress on autophagy.
