Cited by 77Muscle Physiology and DisordersAutophagy in Disease and TherapyMuscle metabolism and nutrition

Role of Autophagy in COPD Skeletal Muscle Dysfunction

Hussain, Sabah N. A., Sandri, Marco·2013·Journal of Applied Physiology

Abstract

Chronic obstructive pulmonary disease (COPD) is a debilitating disease caused by parenchymal damage and irreversible airflow limitation. In addition to lung dysfunction, patients with COPD develop weight loss, malnutrition, poor exercise performance, and skeletal muscle atrophy. The latter has been attributed to an imbalance between muscle protein synthesis and protein degradation. Several reports have confirmed that enhanced protein degradation and atrophy of limb muscles of COPD patient is mediated in part through activation of the ubiquitin-proteasome pathway and that this activation is triggered by enhanced production of reactive oxygen species. Until recently, the importance of the autophagy-lysosome pathway in protein degradation of skeletal muscles has been largely ignored, however, recent evidence suggests that this pathway is actively involved in recycling of cytosolic proteins, organelles, and protein aggregates in normal skeletal muscles. The protective role of autophagy in the regulation of muscle mass has recently been uncovered in mice with muscle-specific suppression of autophagy. These mice develop severe muscle weakness, atrophy, and decreased muscle contractility. No information is yet available about the involvement of the autophagy in the regulation of skeletal muscle mass in COPD patients. Pilot experiments on vastus lateralis muscle samples suggest that the autophagy-lysosome system is induced in COPD patients compared with control subjects. In this revi…

Integrity signals

Registry

Crossref · 10.1152/japplphysiol.00893.2012

Cites

76 of 76 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Hussain and colleagues reported an increase in quadricipital LC3BII, Beclin-1, and p62/SQSTM1 at the protein level.

    “By contrast, Hussain and colleagues reported an increase in quadricipital LC3BII, Beclin-1, and p62/SQSTM1 at the protein level [179].”
  • Autophagy-induced lysosomal degradation is an essential process leading to degradation of cytoplasmic portions in lysosomes.

    “A major other proteolytic pathway is autophagy-induced lysosomal degradation, an essential process leading to the degradation of cytoplasmic portions of variable sizes in the lysosomes (see the review by [179]).”

Cites

1 retracted

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Hussain, S. N. A., & Sandri, M.
Affiliations
  • McGill University Health Centre (CA)
  • Veneto Institute of Molecular Medicine (IT)
Corresponding author
Hussain, Sabah N. A.
Venue
Journal of Applied Physiology
Published
2013-05-01
Volume
114
Issue
9
Pages
1273-1281
ISSN
  • 0161-7567 (ISSN-L)
  • 8750-7587
  • 1522-1601
OpenAlex
W2005001992
Cited by
77
References
76
Citations by year
2026: 3 · 2025: 3 · 2024: 3 · 2023: 3 · 2022: 11 · 2021: 4 · 2020: 8 · 2019: 2 · 2018: 7 · 2017: 7 · 2016: 7 · 2015: 5 · 2014: 8 · 2013: 6
FWCI
0.55
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Applied Physiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
Canadian Institutes of Health Research
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 › Cell Biology › Muscle metabolism and nutrition
Keywords
chronic obstructive pulmonary disease, autophagy, autophagy-lysosome pathway, skeletal muscle atrophy, muscle protein degradation, muscle protein synthesis, ubiquitin-proteasome system, reactive oxygen species, muscle mass regulation, vastus lateralis, muscle dysfunction
MeSH terms
Animals, Autophagy, Humans, Models, Biological, Muscle Proteins, Signal Transduction, Muscle, Skeletal, Pulmonary Disease, Chronic Obstructive, Mice, Proteolysis

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review