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Plasticity of Skeletal, Cardiac and Smooth Muscles in COPD: Repair...
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Plasticity of Skeletal, Cardiac and Smooth Muscles in COPD: Repair and Remodeling

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (31 October 2025) | Viewed by 825

Special Issue Editor

Prof. Dr. Joaquim Gea Guiral

E-Mail Website
Guest Editor
Department of Medicine and Life Sciences (MELIS), Universitat Pompeu Fabra (UPF), 08003 Barcelona, Spain
Interests: skeletal muscles in respiratory diseases; biomarkers in COPD and asthma; omics and new biomarkers in COPD; microbiome and respiratory diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Chronic obstructive pulmonary disease (COPD) is characterized by a permanent airway obstruction, impacting the patient’s different muscle groups. On the one hand, respiratory muscles are subjected to increased diverse respiratory loads under unfavorable conditions (shortening of the diaphragm, nutritional deficiencies, hypoxemia and hypercapnia, and drugs). Muscle damage occurs as a consequence, with subsequent repair and remodeling towards a new phenotype, which appears to be more adapted to the circumstances. The final result is an increased capacity to generate an even greater force than healthy subjects when the latter have high lung volumes and a more aerobic phenotype. This situation is very different in the limb muscles. The dyspnea derived from COPD causes patients to reduce their physical activity. This, together with nutritional and endocrine abnormalities also experienced by patients, leads to atrophy and loss of strength and endurance in these muscles, especially in the lower limbs, with or without the added presence of muscle damage. The result is an involutive phenotype that is not adapted to the tasks of daily life (fibrillar atrophy and loss of aerobic capacity), which leads to disability and conditions affecting the survival of patients. This Special Issue in the Cells journal is focused on the different cellular, molecular and functional phenomena occurring in the respiratory and peripheral muscles of patients with COPD.

Prof. Dr. Joaquim Gea Guiral
Guest Editor

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Keywords

  • injury
  • repair
  • adaptation
  • aerobic metabolism
  • muscle mass
  • limb muscles
  • respiratory muscles
  • proteolysis

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Published Papers (2 papers)

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Research

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16 pages, 1409 KB  
Article
Distinct Intramuscular Extracellular Matrix Protein Responses to Exercise Training in COPD and Healthy Adults and Their Association with Muscle Remodeling
by Davina C. M. Simoes, Efpraxia Kritikaki, Gerasimos Terzis and Ioannis Vogiatzis
Cells 2025, 14(21), 1656; https://doi.org/10.3390/cells14211656 - 22 Oct 2025
Viewed by 346
Abstract
Background: The skeletal muscle extracellular matrix (ECM) is critical for muscle force and the regulation of important physiological processes. A growing body of evidence demonstrates that in aging, altered ECM composition profoundly hinders the capacity for muscle adaptation in response to exercise [...] Read more.
Background: The skeletal muscle extracellular matrix (ECM) is critical for muscle force and the regulation of important physiological processes. A growing body of evidence demonstrates that in aging, altered ECM composition profoundly hinders the capacity for muscle adaptation in response to exercise training. We evaluated the pattern of ECM expression in response to exercise training between healthy young participants and patients with chronic obstructive pulmonary disease (COPD), to provide insight into how normal adaptive processes differ under conditions of chronic disease. Methods: Vastus lateralis muscle biopsies from 29 patients (mean ± SD FEV1: 43 ± 16% predicted) and 14 healthy subjects were analyzed before and after an interval exercise training program for myofiber distribution and size. A selection of ECM molecules was quantified using ELISA. Results: Compared to healthy participants, patients exhibited a lower capacity to increase myofiber type I distribution (by 4.7 ± 3.4 vs. 1.3 ± 2.2%) and mean fiber cross-sectional area (by 13.6 ± 3.2 vs. 9.1 ± 1.9%). Exercise training induced a diverse protein expression between the two cohorts in ECMs regulating tissue structure (collagens: up-regulated only in COPD), myogenesis (SPARC: up-regulated only in healthy), necroptosis (tenascin C: up-regulated only in COPD), adherence to muscle-cell precursors (Fibronectin: up-regulated only in healthy) and tissue integrity (biglycan: down-regulated only in COPD). Conclusions: Impaired ECM remodeling may underlie the reduced exercise training muscle adaptation observed in COPD patients. Full article
(This article belongs to the Special Issue Plasticity of Skeletal, Cardiac and Smooth Muscles in COPD: Repair and Remodeling)
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Review

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19 pages, 770 KB  
Review
Biological Mechanisms Involved in Muscle Dysfunction in COPD: An Integrative Damage–Regeneration–Remodeling Framework
by Joaquim Gea, Mauricio Orozco-Levi, Sergi Pascual-Guàrdia, Carme Casadevall, César Jessé Enríquez-Rodríguez, Ramon Camps-Ubach and Esther Barreiro
Cells 2025, 14(21), 1731; https://doi.org/10.3390/cells14211731 - 4 Nov 2025
Viewed by 220
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 [...] Read more.
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) Reduce damage: bronchodilation, lung-volume reduction, oxygen, non-invasive ventilation, early mobilization, pulmonary rehabilitation, neuromuscular stimulation, and corticosteroid stewardship; (II) Enable regeneration: progressive resistance plus high-intensity/heavy-load endurance training; adequate protein and vitamin-D intake, and endocrine correction; and (III) Steer remodeling: increase physical activity (with/without coaching/telecoaching), functional assessment and CT or MRI monitoring, inspiratory-muscle training, and phenotype-guided adjuncts in selected cases. This framework clarifies why lung deflation strategies benefit inspiratory mechanics, whereas limb recovery requires behavioral and metabolic interventions layered onto systemic optimization. Full article
(This article belongs to the Special Issue Plasticity of Skeletal, Cardiac and Smooth Muscles in COPD: Repair and Remodeling)
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