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Published on: April 10, 2019
Tumor Growth Ameliorates Cardiac Dysfunction and Suppresses Fibrosis in a Mouse Model for Duchenne Muscular Dystrophy
Laris Achlaug1, Lama Awwad1, Irina Langier Goncalves1
1Department of Cell Biology and Cancer Science, Ruth and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, P.O. Box 9649, Haifa 31096, Israel.
Abstract:
The interplay between heart failure and cancer represents a double-edged sword. Whereas cardiac remodeling promotes cancer progression, tumor growth suppresses cardiac hypertrophy and reduces fibrosis deposition. Whether these two opposing interactions are connected awaits to be determined. In addition, it is not known whether cancer affects solely the heart, or if other organs are affected as well. To explore the dual interaction between heart failure and cancer, we studied the human genetic disease Duchenne Muscular Dystrophy (DMD) using the MDX mouse model. We analyzed fibrosis and cardiac function as well as molecular parameters by multiple methods in the heart, diaphragm, lungs, skeletal muscles, and tumors derived from MDX and control mice. Surprisingly, cardiac dysfunction in MDX mice failed to promote murine cancer cell growth. In contrast, tumor-bearing MDX mice displayed reduced fibrosis in the heart and skeletal and diaphragm muscles, resulting in improved cardiac function. The latter is at least partially mediated via M2 macrophage recruitment to the heart and diaphragm muscles. Collectively, our data support the notion that the effect of heart failure on tumor promotion is independent of the improved cardiac function in tumor-bearing mice. Reduced fibrosis in tumor-bearing MDX mice stems from the suppression of new fibrosis synthesis and the removal of existing fibrosis. These findings offer potential therapeutic strategies for DMD patients, fibrotic diseases, and cardiac dysfunction.
Insights
Tumor growth in Duchenne Muscular Dystrophy (DMD) mice unexpectedly reduced cardiac fibrosis and improved heart function. This suggests novel therapeutic avenues for DMD and fibrotic conditions.
Area of Science:
- Cardiovascular Biology
- Oncology
- Musculoskeletal Disorders
Background:
- The relationship between heart failure and cancer is complex, with bidirectional influences.
- Cardiac remodeling can promote cancer, while tumors may suppress cardiac hypertrophy and fibrosis.
- The impact of cancer on organs beyond the heart in heart failure models is largely unknown.
Purpose of the Study:
- To investigate the dual interaction between heart failure and cancer using the Duchenne Muscular Dystrophy (DMD) model.
- To determine if cardiac dysfunction in DMD promotes cancer progression.
- To assess the effects of tumor presence on cardiac function, fibrosis, and other organs in DMD mice.
Main Methods:
- Utilized the MDX mouse model for Duchenne Muscular Dystrophy.
- Analyzed cardiac function, fibrosis, and molecular parameters in the heart, diaphragm, lungs, and skeletal muscles.
- Examined tumors from both MDX and control mice.
- Employed multiple analytical methods to assess tissue and cellular changes.
Main Results:
- Cardiac dysfunction in MDX mice did not promote cancer cell growth.
- Tumor-bearing MDX mice exhibited reduced fibrosis in the heart, diaphragm, and skeletal muscles.
- Improved cardiac function in tumor-bearing MDX mice was observed, partly mediated by M2 macrophage recruitment.
- Reduced fibrosis involved suppression of new synthesis and removal of existing fibrotic tissue.
Conclusions:
- The impact of heart failure on tumor promotion is independent of improved cardiac function in tumor-bearing mice.
- Tumor presence in DMD mice leads to significant reduction in fibrosis and improvement in cardiac and muscle function.
- These findings present potential therapeutic strategies for Duchenne Muscular Dystrophy, fibrotic diseases, and cardiac dysfunction.
