Muscle Atrophy and Hypertrophy Signaling in Patients with Chronic Obstructive Pulmonary Disease

Doucet, Mariève; Russell, Aaron P.; Léger, Bertrand; Debigaré, Richard; Joanisse, Denis R.; Caron, Marc-André; Leblanc, Pierre; Maltais, François

doi:10.1164/rccm.200605-704oc

Cited by 206 publications

(213 citation statements)

References 47 publications

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“…These results are interesting when compared with those of Doucet and colleagues (8). Probably, the differences between the present study and the report of Doucet et al (8) could be related to the different lung diseases and models assessed, since in the present study an asthmatic mouse model was studied, whereas Doucet et al (8) evaluated COPD disease in humans. The absence of molecular markers for muscle atrophy in the present OA group could be attributed to the short period (4 weeks) of the allergic sensitization protocol, which may not have been long enough to induce skeletal muscle atrophy.…”

Section: Discussioncontrasting

confidence: 42%

“…However, treadmill training reduced the expression of these genes in all exercised groups, a fact that could be beneficial in cachexia and disuse conditions. Recent studies have shown an increase of molecular markers of muscle atrophy in human COPD (8,9). Doucet and colleagues (8) reported an increase in the activation of muscle atrophy by the up-regulation of atrogin-1 and MuRF1 in the quadriceps muscle of COPD patients.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have shown an increase of molecular markers of muscle atrophy in human COPD (8,9). Doucet and colleagues (8) reported an increase in the activation of muscle atrophy by the up-regulation of atrogin-1 and MuRF1 in the quadriceps muscle of COPD patients. They provided relevant information about a potential molecular mechanism underlying the development of quadriceps muscle atrophy and weakness in these patients, since atrogin-1 and MuRF1 have been found to be markedly up-regulated during cachexia-and disuse-induced atrophy (10)(11)(12).…”

Section: Discussionmentioning

confidence: 99%

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Effects of exercise training on atrophy gene expression in skeletal muscle of mice with chronic allergic lung inflammation

Durigan

Peviani

Russo

et al. 2009

Braz J Med Biol Res

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We evaluated the effects of chronic allergic airway inflammation and of treadmill training (12 weeks) of low and moderate intensity on muscle fiber cross-sectional area and mRNA levels of atrogin-1 and MuRF1 in the mouse tibialis anterior muscle. Six 4-month-old male BALB/c mice (28.5 ± 0.8 g) per group were examined: 1) control, non-sensitized and non-trained (C); 2) ovalbumin sensitized (OA, 20 μg per mouse); 3) non-sensitized and trained at 50% maximum speed -low intensity (PT50%); 4) non-sensitized and trained at 75% maximum speed -moderate intensity (PT75%); 5) OA-sensitized and trained at 50% (OA+PT50%), 6) OA-sensitized and trained at 75% (OA+PT75%). There was no difference in muscle fiber cross-sectional area among groups and no difference in atrogin-1 and MuRF1 expression between C and OA groups. All exercised groups showed significantly decreased expression of atrogin-1 compared to C (1.01 ± 0.2-fold): PT50% = 0.71 ± 0.12-fold; OA+PT50% = 0.74 ± 0.03-fold; PT75% = 0.71 ± 0.09-fold; OA+PT75% = 0.74 ± 0.09-fold. Similarly significant results were obtained regarding MuRF1 gene expression compared to C (1.01 ± 0.23-fold): PT50% = 0.53 ± 0.20-fold; OA+PT50% = 0.55 ± 0.11-fold; PT75% = 0.35 ± 0.15-fold; OA+PT75% = 0.37 ± 0.08-fold. A short period of OA did not induce skeletal muscle atrophy in the mouse tibialis anterior muscle and aerobic training at low and moderate intensity negatively regulates the atrophy pathway in skeletal muscle of healthy mice or mice with allergic lung inflammation.

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Section: Discussioncontrasting

confidence: 42%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Effects of exercise training on atrophy gene expression in skeletal muscle of mice with chronic allergic lung inflammation

Durigan

Peviani

Russo

et al. 2009

Braz J Med Biol Res

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“…In contrast, systemic consequences may be secondary to the lung disease, probably via the release of inflammatory mediators/cytokines from the lung into the systemic circulation (6,10). Muscle wasting in COPD patients is probably one of the best known systemic features, and this may be due to the effects of cytokines from the lungs on skeletal muscle (11,12) …”

Section: Introductionmentioning

confidence: 99%

Prevalence of COPD in Primary Care Clinics: Correlation with Non-Respiratory Diseases

et al. 2008

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Background and Objective Various extrapulmonary effects and comorbidities have been noted to contribute to the burden of chronic obstructive pulmonary disease (COPD). However, the relationship between the prevalence of COPD and non-respiratory diseases has not been well investigated. The aim of the present study was to determine whether or not COPD is different among patients already suffering from other diseases.

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“…Furthermore, limb muscle NF‐κB activity is increased in patients with lung cancer cachexia 41. FOXO mRNA and protein expression are increased in patients with COPD,38, 39, 42, 43, 44, 45 seemingly independent of body composition, although it is noticeable that in all studies, the patient group showed signs of emphysema. In the COPD patient group, FOXO‐1 protein expression was higher in limb muscles than in respiratory muscles, while this difference was not found in controls 46.…”

Section: New Insights In the Pathophysiology Of Muscle Wasting In Chrmentioning

confidence: 86%

Cachexia in chronic obstructive pulmonary disease: new insights and therapeutic perspective

Sanders¹,

Kneppers²,

Bool³

et al. 2015

Journal of Cachexia, Sarcopenia and Muscle

111

101

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Cachexia and muscle wasting are well recognized as common and partly reversible features of chronic obstructive pulmonary disease (COPD), adversely affecting disease progression and prognosis. This argues for integration of weight and muscle maintenance in patient care. In this review, recent insights are presented in the diagnosis of muscle wasting in COPD, the pathophysiology of muscle wasting, and putative mechanisms involved in a disturbed energy balance as cachexia driver. We discuss the therapeutic implications of these new insights for optimizing and personalizing management of COPD‐induced cachexia.

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Muscle Atrophy and Hypertrophy Signaling in Patients with Chronic Obstructive Pulmonary Disease

Cited by 206 publications

References 47 publications

Effects of exercise training on atrophy gene expression in skeletal muscle of mice with chronic allergic lung inflammation

Effects of exercise training on atrophy gene expression in skeletal muscle of mice with chronic allergic lung inflammation

Prevalence of COPD in Primary Care Clinics: Correlation with Non-Respiratory Diseases

Cachexia in chronic obstructive pulmonary disease: new insights and therapeutic perspective

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