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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Exercise training delays cardiac remodeling in a mouse model of cancer cachexia

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Author(s):
Fernandes, L. G. [1, 2] ; Tobias, G. C. [1] ; Paixao, A. O. [1] ; Dourado, P. M. [3] ; Voltarelli, V. A. [1] ; Brum, P. C. [1]
Total Authors: 6
Affiliation:
[1] Univ Sao Paulo, Sch Phys Educ & Sport, Sao Paulo - Brazil
[2] Univ Sao Paulo, Med Sch, Dept Expt Pathophysiol, Sao Paulo - Brazil
[3] Univ Sao Paulo, Clin Hosp, Fac Med, Heart Inst, Sao Paulo - Brazil
Total Affiliations: 3
Document type: Journal article
Source: Life Sciences; v. 260, NOV 1 2020.
Web of Science Citations: 0
Abstract

Aims: We aimed to investigate the impact of cancer cachexia and previous aerobic exercise training (AET) on cardiac function and structure in tumor bearing mice. Main methods: Colon adenocarcinoma cells 26 (CT26) were subcutaneously injected in BALB/c mice to establish robust cancer cachexia model. AET was performed on a treadmill during 45 days, 60 min/5 days per week. Cardiac function was evaluated by echocardiography and cardiac morphology was assessed by light microscopy. The protein expression levels of mitochondrial complex were analyzed by Western blotting. The mRNA levels of genes related to cardiac remodeling and autophagy were analyzed by quantitative Real-Time PCR. Key findings: Our data confirms CT26 tumor bearing mice as a well-characterized and robust model of cancer cachexia. CT26 mice exhibited cardiac remodeling and dysfunction characterized by cardiac atrophy and impaired left ventricle ejection fraction paralleled by cardiac necrosis, inflammation and fibrosis. AET partially reversed the left ventricle ejection fraction and led to significant anti-cardiac remodeling effect associated reduced necrosis, inflammation and cardiac collagen deposition in CT26 mice. Reduced TGF-beta 1 mRNA levels, increased mitochondrial complex IV protein levels and partial recovery of BNIP3 mRNA levels in cardiac tissue were associated with the cardiac effects of AET in CT26 mice. Thus, we suggest AET as a powerful regulator of key pathways involved in cardiac tissue homeostasis in cancer cachexia. Significance: Our study provides a robust model of cancer cachexia, as well as highlights the potential and integrative effects of AET as a preventive strategy for reducing cardiac damage in cancer cachexia. (AU)

FAPESP's process: 14/25830-9 - Contribution of voluntary aerobic physical activity on cancer cachexia mediators in mice
Grantee:Gabriel Cardial Tobias
Support Opportunities: Scholarships in Brazil - Master
FAPESP's process: 15/22814-5 - Cancer and heart: new paradigms of diagnosis and treatment
Grantee:Carlos Eduardo Negrão
Support Opportunities: Research Projects - Thematic Grants
FAPESP's process: 16/22835-5 - Effects of voluntary physical activity on cardiac function and structure in animal models of cancer cachexia
Grantee:Larissa Gonçalves Fernandes
Support Opportunities: Scholarships in Brazil - Master