ArticleRespiratory research2018
Pulmonary inflammation-induced loss and subsequent recovery of skeletal muscle mass require functional poly-ubiquitin conjugation.
Article in Respiratory research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Differentiated skeletal myotubes coupled with bimodal biosensing for dynamic functional evaluation of inflammatory myotube dysfunction.Microsystems & nanoengineering · 2026Article
- Calprotectin and Sarcopenia in COPD: Biomarker, Bystander or Target?Journal of cachexia, sarcopenia and muscle · 2026Article
- 11β-HSD1 determines the extent of muscle atrophy in a model of acute exacerbation of COPD.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting.International journal of molecular sciences · 2023Review
- Pulmonary inflammation-induced alterations in key regulators of mitophagy and mitochondrial biogenesis in murine skeletal muscle.BMC pulmonary medicine · 2020Article
- Chemerin: A Potential Regulator of Inflammation and Metabolism for Chronic Obstructive Pulmonary Disease and Pulmonary Rehabilitation.BioMed research international · 2020Review
- Inflammation and Skeletal Muscle Wasting During Cachexia.Frontiers in physiology · 2020Review
- Altered protein turnover signaling and myogenesis during impaired recovery of inflammation-induced muscle atrophy in emphysematous mice.Scientific reports · 2018Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundPulmonary inflammation in response to respiratory infections can evoke muscle wasting. Increased activity of the ubiquitin (Ub)-proteasome system (UPS) and the autophagy lysosome pathway (ALP) have been implicated in inflammation-induced muscle atrophy. Since poly-Ub conjugation is required for UPS-mediated proteolysis and has been implicated in the ALP, we assessed the effect of impaired ubiquitin conjugation on muscle atrophy and recovery following pulmonary inflammation, and compared activation and suppression of these proteolytic systems to protein synthesis regulation.
methodsPulmonary inflammation was induced in mice by an intratracheal instillation of LPS. Proteolysis (UPS and ALP) and synthesis signaling were examined in gastrocnemius muscle homogenates. Ub-conjugation-dependency of muscle atrophy and recovery was addressed using Ub-K48R (K48R) mice with attenuated poly-ubiquitin conjugation, and compared to UBWT control mice.
resultsPulmonary inflammation caused a decrease in skeletal muscle mass which was accompanied by a rapid increase in expression of UPS and ALP constituents and reduction in protein synthesis signaling acutely after LPS. Muscle atrophy was attenuated in K48R mice, while ALP and protein synthesis signaling were not affected. Muscle mass recovery starting 72 h post LPS, correlated with reduced expression of UPS and ALP constituents and restoration of protein synthesis signaling. K48R mice however displayed impaired recovery of muscle mass.
conclusionPulmonary inflammation-induced muscle atrophy is in part attributable to UPS-mediated proteolysis, as activation of ALP- and suppression of protein synthesis signaling occur independently of poly-Ub conjugation during muscle atrophy. Recovery of muscle mass following pulmonary inflammation involves inverse regulation of proteolysis and protein synthesis signaling, and requires a functional poly-Ub conjugation.
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