Tumor Growth Ameliorates Cardiac Dysfunction
Lama Awwad1, Rona Shofti2, Tali Haas2
1Department of Cell Biology and Cancer Science, Ruth and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa 3525422, Israel.
Cells
|July 29, 2023
Summary
Cancer progression surprisingly improves heart function during pressure overload. Tumors promote beneficial M1-to-M2 macrophage polarization in the heart, reducing cardiac hypertrophy and fibrosis, but this effect requires functional macrophages.
Area of Science:
- Cardiovascular Biology
- Oncology
- Immunology
Background:
- Heart failure and cancer are leading global causes of mortality.
- Cardiac dysfunction is known to exacerbate cancer progression and metastasis.
- The impact of tumor progression on cardiac remodeling remains largely unexplored.
Purpose of the Study:
- To investigate the effects of tumor progression on cardiac remodeling under pressure overload.
- To identify the mechanisms by which tumors influence cardiac adaptation to stress.
Main Methods:
- Utilized a transverse aortic constriction (TAC) mouse model to induce pressure overload.
- Introduced proliferating cancer cells (two different lines) into TAC-operated mice.
- Performed integrative analysis including qRT-PCR, flow cytometry, and immunofluorescence.
Main Results:
- Tumor-bearing mice exhibited reduced cardiac hypertrophy and fibrosis following TAC.
- Cardiac contractile function was improved in tumor-bearing mice post-TAC.
- Tumor-dependent M1-to-M2 macrophage polarization in the heart mediated these beneficial effects.
- Macrophage depletion abolished the protective effects of tumors on cardiac function and fibrosis.
Conclusions:
- Tumor progression can beneficially modulate cardiac remodeling in response to pressure overload.
- Cardiac macrophage polarization is a key mechanism linking cancer and improved cardiac outcomes.
- Targeting cardiac macrophages may offer novel therapeutic strategies for heart failure patients with cancer.
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