Systemic inflammation is associated with mitophagy signalling in skeletal muscle of COPD patients
Abstract
Loss of skeletal muscle mitochondrial content is an important extra-pulmonary manifestation of COPD, of which the cause is only partly understood. Pre-clinical research indicates that systemic inflammation induces mitochondrial breakdown (mitophagy). Hence, we hypothesise that skeletal muscle of COPD patients characterized by systemic inflammation exhibits a pro-mitophagy gene and protein expression profile associated with loss of mitochondrial content. Vastus lateralis biopsies were obtained of COPD patients, and high sensitive serum C-reactive protein (CRP) levels were determined by ELISA as a marker of systemic inflammation. Patients were categorised by high (CRP+; N=9; CRP>3.0 mg/L) or low (CRP-; N=19; CRP≤3.0 mg/L) systemic inflammation. Mitochondrial content was assessed by quantification of multiple subunits of the oxidative phosphorylation complexes and the mtDNA/gDNA ratio. General autophagy- (LC3B, GABARAPL1, SQSTM1) and mitophagy- (BNIP3L, BNIP3, FUNDC1, Parkin) associated protein and mRNA levels were quantified. Protein levels of BNIP3 (p=0.009), LC3BI (p=0.095), and LC3BII (p=0.048) were higher, and GABARAPL1 (p=0.098), and SQSTM1 (p=0.054) tended to be higher in CRP+. No differences in gene-expression of these markers, or of mitochondrial content markers were found between the CRP+ and CRP- group. It can be concluded that enhanced BNIP3-mediated mitophagy signalling in skeletal muscle of COPD patients is associated with an elevated systemic inflammatory status.…
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In COPD patients with high circulating C-reactive protein (CRP), BNIP3 protein level is increased in muscle compared to other COPD patients, indicating mitophagy is associated with systemic inflammation.
“Finally, the same team performed a similar study in COPD patients according to their inflammatory status and found an increase in BNIP3 at the protein level in COPD patients with high circulating C-reactive protein (CRP) compared to other COPD patients, pointing out that mitophagy was associated with systemic inflammation [110].”
From Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting (2023) · cites this paper as [110]
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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
“Finally, the same team performed a similar study in COPD patients according to their inflammatory status and found an increase in BNIP3 at the protein level in COPD patients with high circulating C-reactive protein (CRP) compared to other COPD patients, pointing out that mitophagy was associated with systemic inflamma…”
Result
- Authors
- Gosker, H. R., Leermakers, P. A., Kneppers, A. E., Kelders, M. C., De Theije, C. C., & Schols, A. M.
- Affiliations
- Maastricht University Medical Centre (NL)
- Venue
- Molecular Pathology and Funct. Genomics
- Publisher
- European Respiratory Society
- Published
- 2018-09-15
- Pages
- PA932
- OpenAlex
- W2906186698
- 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 › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- chronic obstructive pulmonary disease, systemic inflammation, mitophagy, skeletal muscle, mitochondrial content, C-reactive protein, BNIP3, LC3B, GABARAPL1, p62, autophagy, oxidative phosphorylation complexes, extrapulmonary manifestations
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