ReviewCells2025
Biological Mechanisms Involved in Muscle Dysfunction in COPD: An Integrative Damage-Regeneration-Remodeling Framework.
Review in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed.
- Current evidence and emerging therapeutic strategies for non-exercise interventions in sarcopenia associated with chronic obstructive pulmonary disease: a narrative review.Journal of thoracic disease · 2026Review
- Gastroesophageal reflux disease predicts 6-month readmission in acute exacerbation of chronic obstructive pulmonary disease: development and validation of a nomogram.Journal of thoracic disease · 2026Article
- Article
- Mitochondrial and Epigenetic Drivers of Skeletal Muscle Dysfunction in Chronic Obstructive Pulmonary Disease.Antioxidants (Basel, Switzerland) · 2026Review
- Frailty and COPD: a bidirectional relationship in the context of systemic and accelerated ageing.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Sarcopenia and Frailty in COPD: Mechanisms, Relationship with Malnutrition and Potential Therapeutic Interventions.Nutrients · 2026Review
- Sex-Specific Plasma Metabolomic Signatures in COPD Reveal Creatine, Purine/Urate, and Bile-Acid Axes.Metabolites · 2026Article
- Multimodal Therapeutic Strategies for the Management of Sarcopenia and Frailty in Chronic Obstructive Pulmonary Disease: A Narrative Review.Nutrients · 2026Review
- Beyond blood gases: diaphragm-guided sequential non-invasive ventilation for COPD with type II respiratory failure.Frontiers in medicine · 2026Review
- Mechanical Forces and Mechanotransduction in COPD: Pathogenesis, Clinical Phenotypes, and Therapeutic Implications.International journal of chronic obstructive pulmonary disease · 2026Review
- Diagnostic value of geriatric nutritional risk index and phase angle for malnutrition in patients with COPD: a retrospective cohort study.Frontiers in nutrition · 2026Article
- Sarcopenia trajectories and associated factors after lung transplantation: a growth mixture model study.Frontiers in medicine · 2026Article
- Development of an opportunistic chest CT-based nomogram for identifying low muscle mass in hospitalized patients with COPD.Frontiers in medicine · 2026Article
- Mitochondrial Mechanisms of Resistance Exercise in COPD-Related Skeletal Muscle Dysfunction: A Narrative Review.International journal of chronic obstructive pulmonary disease · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Skeletal muscle dysfunction is a major systemic manifestation of COPD that shapes symptoms, exercise tolerance and mortality. Current evidence can be integrated within a Damage-Regeneration-Remodeling framework linking mechanics and biology to clinical phenotypes. Pulmonary hyperinflation and chest wall geometry chronically load the diaphragm and other respiratory muscles in COPD, whereas inactivity and exacerbation-related disuse underload locomotor muscles. Across muscle compartments, oxidative/nitrosative stress, activation of proteolytic pathways, mitochondrial and endoplasmic reticulum stress, microvascular limitations, neuromuscular junction instability, and myosteatosis degrade muscle quality. The diaphragm adapts with a fast-to-slow fiber shift, greater oxidative capacity, and sarcomere foreshortening, improving endurance, whereas limb muscles show atrophy, a glycolytic shift, reduced oxidative enzymes, extracellular matrix accrual, and fat infiltration. Translational levers that address these mechanisms include: (I)
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.