Impaired coordination of skeletal muscle protein turnover signalling in sarcopenic COPD patients
Abstract
Background: The prevalence of sarcopenia is high in advanced COPD. Although in muscle atrophy an imbalance between anabolism and catabolism is evident, data on regulation of muscle protein turnover in COPD is conflicting. Therefore, we studied molecular signatures of protein turnover in a large, well-phenotyped cohort. Methods: Quadriceps muscle biopsies were obtained from 91 COPD patients and 14 healthy control subjects (C), recruited in Maastricht (NLD) and Golnik (SLV). Sarcopenia was assessed by DEXA. Protein and mRNA levels of regulatory constituents of muscle maintenance were analyzed. Results: Patients were clustered by sarcopenia (Yes: S (N=39); No: NS (N=52)). Muscle maintenance regulatory constituents are depicted in Table 1. Conclusion: Protein synthesis signalling is increased despite reduced AKT activity in sarcopenic COPD patients. Autophagy appears induced, while ubiquitin-proteasome system regulation is unaltered. This impaired coordination of protein synthesis and proteolytic signalling, despite activation of myogenesis, may contribute to muscle loss in COPD.
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A study on quadriceps of 91 COPD patients showed that Akt phosphorylation was decreased in COPD compared to healthy subjects as well as in sarcopenic versus nonsarcopenic patients; however, other markers of protein synthesis signaling such as S6- or 4EBP1-phosphorylations were increased in both cases.
“For example, a study performed on the quadriceps of 91 COPD patients showed that Akt phosphorylation was decreased in COPD compared to healthy subjects as well as in sarcopenic versus nonsarcopenic patients. However, other markers of protein synthesis signaling such as S6- or 4EBP1-phosphorylations were increased in both cases [188].”
From Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting (2023) · cites this paper as [188]
This study did not evidence any increased activity of the ubiquitin-proteasome pathway in COPD or sarcopenic patients.
“Of note, this study did not evidence any increased activity of the ubiquitin–proteasome pathway in COPD or sarcopenic patients.”
From Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting (2023) · cites this paper as [188]
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Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting
Henrot, P., Dupin, I., Schilfarth, P., Esteves, P., Blervaque, L., Zysman, M., Gouzi, F., Hayot, M., Pomiès, P., & Berger, P. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24076454 · Cited by 85 · see citing works
“However, other markers of protein synthesis signaling such as S6- or 4EBP1-phosphorylations were increased in both cases [188].”
Background
- Authors
- Kneppers, A., Langen, R., Gosker, H., Leermakers, P., Kelders, M., de Theye, C., Cebron Lipovec, N., Omersa, D., Lainscak, M., & Schols, A.
- Affiliations
- Maastricht University Medical Centre (NL)
- National Institute of Public Health (JP)
- Venue
- 3.1 Molecular Pathology and Functional Genomics
- Publisher
- European Respiratory Society
- Published
- 2016-09
- Pages
- PA3400
- OpenAlex
- W2557018593
- Cited by
- 1
- References
- 0
- Citations by year
- 2023: 1
- Type
- conference abstract
- Language
- en
- Open access
- closed
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Physiology › Nutrition and Health in Aging
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
- Keywords
- sarcopenia, chronic obstructive pulmonary disease, skeletal muscle protein turnover, muscle atrophy, Akt signaling, autophagy, ubiquitin-proteasome system, myogenesis, quadriceps
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