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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 prevents impaired autophagy and proteostasis in a model of neurogenic myopathy

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Campos, Juliane C. [1] ; Baehr, Leslie M. [2] ; Gomes, Katia M. S. [1] ; Bechara, Luiz R. G. [1] ; Voltarelli, Vanessa A. [3] ; Bozi, Luiz H. M. [1] ; Ribeiro, Marcio A. C. [1] ; Ferreira, Nikolas D. [1] ; Moreira, Jose B. N. [3, 4] ; Brum, Patricia C. [3] ; Bodine, Sue C. [2] ; Ferreira, Julio C. B. [1]
Total Authors: 12
[1] Univ Sao Paulo, Inst Biomed Sci, BR-05508000 Sao Paulo - Brazil
[2] Univ Iowa, Endocrinol & Metab Div, Dept Internal Med, Iowa City, IA 52242 - USA
[3] Univ Sao Paulo, Sch Phys Educ & Sport, BR-05508030 Sao Paulo - Brazil
[4] Norwegian Univ Sci & Technol, Fac Med & Hlth Sci, Cardiac Exercise Res Grp, N-7006 Trondheim - Norway
Total Affiliations: 4
Document type: Journal article
Source: SCIENTIFIC REPORTS; v. 8, AUG 7 2018.
Web of Science Citations: 4

Increased proteolytic activity has been widely associated with skeletal muscle atrophy. However, elevated proteolysis is also critical for the maintenance of cellular homeostasis by disposing cytotoxic proteins and non-functioning organelles. We recently demonstrated that exercise activates autophagy and re-establishes proteostasis in cardiac diseases. Here, we characterized the impact of exercise on skeletal muscle autophagy and proteostasis in a model of neurogenic myopathy induced by sciatic nerve constriction in rats. Neurogenic myopathy, characterized by progressive atrophy and impaired contractility, was paralleled by accumulation of autophagy-related markers and loss of acute responsiveness to both colchicine and chloroquine. These changes were correlated with elevated levels of damaged proteins, chaperones and pro-apoptotic markers compared to control animals. Sustained autophagy inhibition using chloroquine in rats (50 mg. kg(-1). day(-1)) or muscle-specific deletion of Atg7 in mice was sufficient to impair muscle contractility in control but not in neurogenic myopathy, suggesting that dysfunctional autophagy is critical in skeletal muscle pathophysiology. Finally, 4 weeks of aerobic exercise training (moderate treadmill running, 5x/week, 1 h/day) prior to neurogenic myopathy improved skeletal muscle autophagic flux and proteostasis. These changes were followed by spared muscle mass and better contractility properties. Taken together, our findings suggest the potential value of exercise in maintaining skeletal muscle proteostasis and slowing down the progression of neurogenic myopathy. (AU)

FAPESP's process: 12/14416-1 - Protein quality control profile in skeletal muscle wasting: role of beta2- adrenergic receptor
Grantee:Juliane Cruz Campos
Support Opportunities: Scholarships in Brazil - Doctorate
Grantee:Juliane Cruz Campos
Support Opportunities: Scholarships abroad - Research Internship - Doctorate
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: 15/20783-5 - Protein quality control in dysfunctional/atrophic skeletal muscle: role of b2-adrenoceptor
Grantee:Julio Cesar Batista Ferreira
Support Opportunities: Regular Research Grants