Related Experiment Video
Updated: Apr 19, 2026
Activating Autophagy by Aerobic Exercise in Mice
Published on: February 3, 2017
Inhibition of autophagy recovers cardiac dysfunction and atrophy in response to tail-suspension
Hong Liu1, Qiong Xie2, Bing-Mu Xin2
1Department of Oncology, Institute of Medicinal Biotechnology, Peking Union Medical College, Chinese Academy of Medical Sciences, 1# Tiantan Xili, Beijing 100050, PR China.
Insights
Physical inactivity causes cardiac dysfunction and atrophy by increasing autophagy. Inhibiting autophagy with chloroquine reversed these effects, suggesting autophagy is a therapeutic target for inactivity-induced heart disease.
Area of Science:
- Cardiovascular Physiology
- Cellular Biology
- Space Medicine
Background:
- Physical inactivity during space flight or bed rest leads to cardiac dysfunction and atrophy.
- The precise mechanisms regulating myocardial dysfunction and atrophy due to inactivity are not fully understood.
- Autophagy, a cellular degradation process, is implicated in cardiac dysfunction and atrophy.
Purpose of the Study:
- To investigate the relationship between inactivity-induced cardiac dysfunction and atrophy and autophagy in rat cardiac tissue.
- To explore the role of autophagy in the progression of cardiac atrophy and dysfunction caused by physical inactivity.
Main Methods:
- Simulated physical inactivity using a rat tail suspension model.
- Assessed cardiac function via echocardiography.
- Quantified cardiac atrophy using wheat germ agglutinin staining.
- Measured autophagic activity through Western blot and immunofluorescence staining.
Main Results:
- Tail suspension led to decreased cardiac function (contractility) and increased cardiac atrophy.
- Myocardial cell cross-sectional area reduced, but apoptosis did not increase.
- Autophagy markers (proteins, autophagosomes) were elevated in tail-suspended hearts.
- Chloroquine administration reversed cardiac dysfunction and atrophy by suppressing autophagy.
Conclusions:
- Autophagy plays a crucial role in facilitating cardiac dysfunction and atrophy induced by physical inactivity.
- Autophagy-related signaling pathways represent potential therapeutic targets for treating cardiac conditions arising from physical inactivity.
Aims:
Physical inactivity during space flight or prolonged bed rest may cause cardiac dysfunction and atrophy, but the exact mechanism that governs the regulation of myocardial dysfunction and cardiac atrophy remains poorly understood. Autophagy, a protein degradation pathway, has recently been shown to be involved in the regulation of cardiac dysfunction and atrophy. In this study, we investigated the relationships between dysfunction and inactivity-induced atrophy and autophagy in rat cardiac tissue.
Main Methods:
Physical inactivity was simulated by a tail suspension model, and cardiac function was examined by echocardiography. Cardiac atrophy was measured by wheat germ agglutinin staining and autophagic activity was detected by Western blot analysis and immunofluorescence staining.
Key Findings:
We demonstrated that cardiac function, especially contractility, declined and the area of cardiac atrophy increased in the tail-suspended cardiac tissue. Additionally, the cross-sectional area of myocardial cells decreased; however, apoptosis did not increase with tail suspension. Similarly, the expression of autophagy-related proteins and the number of autophagosomes were elevated in the tail-suspended cardiac tissue. Moreover, the administration of chloroquine, an autophagy inhibitor, reversed cardiac dysfunction and atrophy via the suppression of autophagic activity during suspension. Our results indicate that autophagy facilitates the development and progression of cardiac dysfunction and atrophy induced by tail suspension.
Significance:
Our studies hint that the components of the autophagy-related signaling pathway are potential therapeutic targets for the treatment of cardiac diseases induced by physical inactivity.
