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Effects of voluntary physical activity on cardiac function and structure in animal models of cancer cachexia

Grant number: 16/22835-5
Support type:Scholarships in Brazil - Master
Effective date (Start): March 01, 2017
Effective date (End): February 28, 2019
Field of knowledge:Health Sciences - Physical Education
Cooperation agreement: Coordination of Improvement of Higher Education Personnel (CAPES)
Principal Investigator:Patricia Chakur Brum
Grantee:Larissa Gonçalves Fernandes
Home Institution: Escola de Educação Física e Esporte (EEFE). Universidade de São Paulo (USP). São Paulo , SP, Brazil
Associated research grant:15/22814-5 - Cancer and heart: new paradigms of diagnosis and treatment, AP.TEM

Abstract

Cancer cachexia is a complex multifactorial syndrome associated with reduced quality of life and increased mortality. It is characterized mainly by the loss of body mass that results in the progressive functional disability of the patient (Tisdale, 2010). Although most studies have prioritized the mechanisms related to the loss of skeletal muscle mass in cancer cachexia, there is a growing interest in changes in the heart muscle promoted by tumor action, regardless of therapeutic interventions, and which contribute significantly to the mortality of cancer patients. Cancer cachexia-induced cardiac dysfunction represents a poorly explored component, and possible mechanisms and functional implications have not been fully characterized in tumor models. In addition, the effect of physical activity on cardiac function and structure in these models has not yet been studied. In this context, we hypothesized that physical activity would be able to attenuate the deleterious effects of cancer on cardiac function and structure. Therefore, the objective of this project will be to investigate the effects of voluntary physical activity on cardiac function and structure in different mouse models of cancer cachexia. In this way, we will answer the following questions: 1) are the proposed experimental models accompanied by cardiac dysfunction and abnormalities in cardiac structure? 2) Is the level of previous physical activity able to attenuate cardiac dysfunction and cardiac remodeling caused by cancer-induced cachexia? For this, mice will be exposed to a wheel running and then inoculated with Lewis lung carcinoma (LLC) or colon carcinoma (CT26) tumor cells. We will perform cardiac function and structure by echocardiography, cardiac histological analysis, and expression of cardiac remodeling genes. (AU)