{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T21:15:06Z","timestamp":1792444506569,"version":"4.5.0"},"reference-count":40,"publisher":"European Respiratory Society (ERS)","issue":"3","license":[{"start":{"date-parts":[[2024,5,1]],"date-time":"2024-05-01T00:00:00Z","timestamp":1714521600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["publications.ersnet.org"],"crossmark-restriction":true},"short-container-title":["ERJ Open Res"],"accepted":{"date-parts":[[2024,3,2]]},"published-print":{"date-parts":[[2024,5]]},"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>Extracellular matrix (ECM) proteins are the major constituents of the muscle cell micro-environment, imparting instructive signalling, steering cell behaviour and controlling muscle regeneration. ECM remodelling is among the most affected signalling pathways in COPD and aged muscle. As a fraction of COPD patients present muscle atrophy, we questioned whether ECM composition would be altered in patients with peripheral muscle wasting (atrophic COPD) compared to those without muscle wasting (non-atrophic COPD).<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>A set of ECM molecules with known impact on myogenesis were quantified in vastus lateralis muscle biopsies from 29 COPD patients (forced expiratory volume in 1\u2005s 55\u00b112% predicted) using ELISA and real-time PCR. COPD patients were grouped to atrophic or non-atrophic based on fat-free mass index (&lt;17 or \u226517\u2005kg\u00b7m<jats:sup>\u22122<\/jats:sup>).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Atrophic COPD patients presented a lower average vastus lateralis muscle fibre cross-sectional area (3872\u00b1258\u2005\u03bcm<jats:sup>2<\/jats:sup>) compared to non-atrophic COPD (4509\u00b1198\u2005\u03bcm<jats:sup>2<\/jats:sup>). Gene expression of ECM molecules was found significantly lower in atrophic COPD compared to non-atrophic COPD for collagen type I alpha 1 chain (<jats:italic>COL1A1<\/jats:italic>), fibronectin (<jats:italic>FN1<\/jats:italic>), tenascin C (<jats:italic>TNC<\/jats:italic>) and biglycan (<jats:italic>BGN<\/jats:italic>)<jats:italic>.<\/jats:italic>In terms of protein levels, there were no significant differences between the two COPD cohorts for any of the ECM molecules tested.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Although atrophic COPD presented decreased contractile muscle tissue, the differences in ECM mRNA expression between atrophic and non-atrophic COPD were not translated at the protein level, potentially indicating an accumulation of long-lived ECM proteins and dysregulated proteostasis, as is typically observed during deconditioning and 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