Excessive training induces molecular signs of pathologic cardiac hypertrophy
| Autor: | Lilian Eslaine Costa Mendes da Silva, José Rodrigo Pauli, Dennys E. Cintra, Rania A. Mekary, Luciana da C Oliveira, Ellen Cristini de Freitas, Gustavo P. Morais, Alisson L. da Rocha, Adelino Sanchez Ramos da Silva, Giovana R. Teixeira, Eduardo R. Ropelle, Larissa G. de Vicente, Ana P. Pinto, Leandro Pereira de Moura |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Physiology Cardiac fibrosis Clinical Biochemistry Cardiomegaly Myostatin 030204 cardiovascular system & hematology Left ventricular hypertrophy Proinflammatory cytokine Muscle hypertrophy 03 medical and health sciences Mice 0302 clinical medicine Receptors Glucocorticoid AMP-Activated Protein Kinase Kinases Fibrosis Internal medicine Physical Conditioning Animal medicine Animals Humans Mechanistic target of rapamycin Inflammation Nonmuscle Myosin Type IIB biology Myosin Heavy Chains business.industry Interleukin-6 Cell Biology medicine.disease Disease Models Animal 030104 developmental biology Endocrinology Receptors Androgen Heart failure biology.protein Hypertrophy Left Ventricular business Protein Kinases |
| Zdroj: | Journal of cellular physiology. 233(11) |
| ISSN: | 1097-4652 |
| Popis: | Chronic exercise induces cardiac remodeling that promotes left ventricular hypertrophy and cardiac functional improvement, which are mediated by the mammalian or the mechanistic target of rapamycin (mTOR) as well as by the androgen and glucocorticoid receptors (GRs). However, pathological conditions (i.e., chronic heart failure, hypertension, and aortic stenosis, etc.) also induce cardiac hypertrophy, but with detrimental function, high levels of proinflammatory cytokines and myostatin, elevated fibrosis, reduced adenosine monophosphate-activated protein kinase (AMPK) activation, and fetal gene reactivation. Furthermore, recent studies have evidenced that excessive training induced an inflammatory status in the serum, muscle, hypothalamus, and liver, suggesting a pathological condition that could also be detrimental to cardiac tissue. Here, we verified the effects of three running overtraining (OT) models on the molecular parameters related to physiological and pathological cardiac hypertrophy. C57BL/6 mice performed three different OT protocols and were evaluated for molecular parameters related to physiological and pathological cardiac hypertrophy, including immunoblotting, reverse transcription polymerase chain reaction, histology, and immunohistochemistry analyses. In summary, the three OT protocols induced left ventricle (LV) hypertrophy with signs of cardiac fibrosis and negative morphological adaptations. These maladaptations were accompanied by reductions in AMPKalpha (Thr172) phosphorylation, androgen receptor, and GR expressions, as well as by an increase in interleukin-6 expression. Specifically, the downhill running-based OT model reduced the content of some proteins related to the mTOR signaling pathway and upregulated the β-isoform of myosin heavy-chain gene expression, presenting signs of LV pathological hypertrophy development. |
| Databáze: | OpenAIRE |
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