Abstract
Abstract
Heart failure and cancer are the most deadly diseases worldwide. Murine models for cardiac remodeling and heart failure demonstrate that cardiac dysfunction promotes cancer progression and metastasis spread. Yet, no information is available on whether and how tumor progression affects cardiac remodeling. Here, we examined cardiac remodeling following transverse aortic constriction in the presence or absence of proliferating cancer cells. We show that tumor-bearing mice display reduced cardiac hypertrophy, lower fibrosis and improved cardiac contractile function. We further identify tumor-dependent M1-to-M2 polarization in the cardiac macrophage population as a mediator of the beneficial tumor effect on the heart. Harnessing cancer paradigms that are involved in tumor-dependent improved cardiac outcome may provide novel therapeutic strategies for cardiovascular diseases.
Publisher
Research Square Platform LLC
Cited by
2 articles.
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