Respiratory Research最新文献

{"title":"Correction: Precision cut lung slices: an integrated ex vivo model for studying lung physiology, pharmacology, disease pathogenesis and drug discovery.","authors":"Cynthia Koziol-White, Eric Gebski, Gaoyaun Cao, Reynold A Panettieri","doi":"10.1186/s12931-024-03085-6","DOIUrl":"10.1186/s12931-024-03085-6","url":null,"abstract":"","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"42"},"PeriodicalIF":5.8,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11773737/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143053943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HMOX1 as a potential drug target for upper and lower airway diseases: insights from multi-omics analysis.","authors":"Enhao Wang, Shazhou Li, Yang Li, Tao Zhou","doi":"10.1186/s12931-025-03124-w","DOIUrl":"10.1186/s12931-025-03124-w","url":null,"abstract":"<p><strong>Background: </strong>Oxidative stress is key in inflammatory airway diseases. Heme oxygenase 1 (HMOX1) regulates oxidative stress, but its role in airway diseases needs exploration.</p><p><strong>Methods: </strong>Differentially expressed genes (DEGs) between healthy nasal mucosa and chronic rhinosinusitis with nasal polyps (CRSwNP) were identified from Gene Expression Omnibus (GEO). Candidate genes were further screened using Gene Set Enrichment Analysis (GSEA) and Random Forest (RF) algorithms. Causal inference between candidate genes and upper and lower airway diseases (CRSwNP, allergic rhinitis (AR), and asthma (AS)) was conducted using bidirectional two-sample Mendelian randomization (TwoSampleMR) analysis. Single-cell RNA sequencing (scRNA-seq) data were used to determine the cellular localization and intercellular interactions of candidate genes. Molecular docking was used to identify potential therapeutic agents.</p><p><strong>Results: </strong>HMOX1 expression was significantly elevated in CRSwNP. TwoSampleMR analysis indicated a negative causal relationship between HMOX1 exposure and the occurrence of upper and lower airway diseases (CRSwNP [(odds ratio (OR)/95% confidence interval (CI): 0.945/(0.893-0.999), P = 0.044], AR [OR/95% CI: 0.997/(0.994-0.999), P = 0.007], and AS [OR/95% CI: 0.935/(0.895-0.977), P = 0.003]). scRNA-seq data revealed HMOX1 localization in M2 macrophages. Molecular docking identified 15 antioxidants, including Acetylcysteine and Quercetin, that can upregulate HMOX1 expression.</p><p><strong>Conclusion: </strong>HMOX1 may have a protective role in the pathogenesis of upper and lower airway diseases (CRSwNP, AR, and AS) by modulating oxidative stress. Antioxidants that increase HMOX1 expression could offer new therapeutic avenues for these diseases.</p><p><strong>Clinical trial: </strong>Not applicable.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"41"},"PeriodicalIF":5.8,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11773792/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143053944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Peripheral blood miRNAs are associated with airflow below threshold in children with asthma.","authors":"Anshul Tiwari, Brian D Hobbs, Rinku Sharma, Jiang Li, Alvin T Kho, Sami Amr, Juan C Celedón, Scott T Weiss, Craig P Hersh, Kelan G Tantisira, Michael J McGeachie","doi":"10.1186/s12931-025-03116-w","DOIUrl":"10.1186/s12931-025-03116-w","url":null,"abstract":"<p><strong>Background: </strong>MicroRNAs (miRNAs) are crucial post-transcriptional regulators involved in inflammatory diseases, such as asthma. Poor lung function and airflow issues in childhood are linked to the development of chronic obstructive pulmonary disease (COPD) in adulthood.</p><p><strong>Methods: </strong>We analyzed small RNA-Seq data from 365 peripheral whole blood samples from the Genetics of Asthma in Costa Rica Study (GACRS) for association with airflow levels measured by FEV1/FVC. Differentially expressed (DE) miRNAs were identified using DESeq2 in R, adjusting for covariates and applying a 10% false discovery rate (FDR). The analysis included 361 samples and 649 miRNAs. The two DE miRNAs were further tested for association with airflow obstruction in a study of adult former smokers with and without COPD.</p><p><strong>Results: </strong>We found 1 upregulated and 1 downregulated miRNA in participants with airflow below the threshold compared to those above it. In the adult study, the same miRNAs were upregulated and downregulated in individuals with FEV1/FVC < 0.7 versus those with FEV1/FVC > 0.7, showing suggestive statistical evidence. The target genes of these miRNAs were enriched for PI3K-Akt, Hippo, WNT, MAPK, and focal adhesion pathways.</p><p><strong>Conclusions: </strong>Two differentially expressed miRNAs were associated with airflow levels in children with asthma and airflow obstruction in adults with COPD. This suggests that shared genetic regulatory systems may influence childhood airflow and contribute to adulthood airflow obstruction.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"38"},"PeriodicalIF":5.8,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11763123/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143041923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single, double, and triple-hit strategies to establish a long-term premature rabbit model of bronchopulmonary dysplasia.","authors":"Chiara Catozzi, Francesca Stretti, Enrica Scalera, Matteo Storti, Angelo Modena, Giorgio Aquila, Gino Villetti, Erica Ferrini, Andrea Grandi, Franco Fabio Stellari, Francesca Ravanetti, Luisa Ragionieri, Roberta Ciccimarra, Matteo Zoboli, Christina Brandenberger, Henri Schulte, Xabier Murgia, Maurizio Civelli, Francesca Ricci","doi":"10.1186/s12931-024-03053-0","DOIUrl":"10.1186/s12931-024-03053-0","url":null,"abstract":"<p><strong>Background: </strong>Bronchopulmonary dysplasia (BPD) is a chronic lung condition of premature neonates, yet without an established pharmacological treatment. The BPD rabbit model exposed to 95% oxygen has been used in recent years for drug testing. However, the toxicity of the strong hyperoxic hit precludes a longer-term follow-up due to high mortality after the first week of life. This study aimed to extend the preterm rabbit model to postnatal day (PND) 14 to mimic the evolving phase of BPD and enable the investigation of therapeutic interventions at later and more relevant time points.</p><p><strong>Methods: </strong>Preterm rabbit pups delivered on the 28th day of gestation were either exposed to room air or different degrees of hyperoxia (50% and 70% O₂) for 14 days. Single (immediately after birth) or double (at birth and at PND5) intratracheal lipopolysaccharide (LPS) administrations were also tested in combination with 50% O₂. Age-matched rabbits delivered vaginally at term were used as controls. Survival, weight gain, lung function, pulmonary artery micro-ultrasound Doppler analysis, lung histology (alveolarization, lung injury score, and design-based stereology), and longitudinal micro-CT imaging were used to compare the outcomes at PND14.</p><p><strong>Results: </strong>Premature birth itself, without any other BPD hit, was associated with lung function deficits, delayed lung development, and cardiovascular abnormalities. The BPD-like lung phenotype was enhanced by 70% O₂ but not by 50% O₂ hyperoxia. Intratracheal LPS delivered immediately after birth was associated with significantly higher lung injury scores at PND14 and increased tissue damping, a marker of parenchymal air resistance.</p><p><strong>Conclusion: </strong>Several strategies are feasible to extend the preterm rabbit model of BPD to PND14. Preterm birth at the saccular phase itself, even in the absence of other postnatal BPD hits, was associated with lung function deficits, delayed lung development, and cardiovascular abnormalities compared with age-matched term rabbit pups. Enhanced BPD-like phenotypes can be further achieved by continued exposure to moderate hyperoxia (70% O₂) and the intratracheal administration of LPS.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"35"},"PeriodicalIF":5.8,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11762538/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143042318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Automated AI-based image analysis for quantification and prediction of interstitial lung disease in systemic sclerosis patients.","authors":"Julien Guiot, Monique Henket, Fanny Gester, Béatrice André, Benoit Ernst, Anne-Noelle Frix, Dirk Smeets, Simon Van Eyndhoven, Katerina Antoniou, Lennart Conemans, Janine Gote-Schniering, Hans Slabbynck, Michael Kreuter, Jacobo Sellares, Ioannis Tomos, Guang Yang, Clio Ribbens, Renaud Louis, Vincent Cottin, Sara Tomassetti, Vanessa Smith, Simon L F Walsh","doi":"10.1186/s12931-025-03117-9","DOIUrl":"10.1186/s12931-025-03117-9","url":null,"abstract":"<p><strong>Background: </strong>Systemic sclerosis (SSc) is a rare connective tissue disease associated with rapidly evolving interstitial lung disease (ILD), driving its mortality. Specific imaging-based biomarkers associated with the evolution of lung disease are needed to help predict and quantify ILD.</p><p><strong>Methods: </strong>We evaluated the potential of an automated ILD quantification system (icolung^®) from chest CT scans, to help in quantification and prediction of ILD progression in SSc-ILD. We used a retrospective cohort of 75 SSc-ILD patients to evaluate the potential of the AI-based quantification tool and to correlate image-based quantification with pulmonary function tests and their evolution over time.</p><p><strong>Results: </strong>We evaluated a group of 75 patients suffering from SSc-ILD, either limited or diffuse, of whom 30 presented progressive pulmonary fibrosis (PPF). The patients presenting PPF exhibited more extensive lesions (in % of total lung volume (TLV)) based on image analysis than those without PPF: 3.93 (0.36-8.12)* vs. 0.59 (0.09-3.53) respectively, whereas pulmonary functional test showed a reduction in Force Vital Capacity (FVC)(pred%) in patients with PPF compared to the others : 77 ± 20% vs. 87 ± 19% (p < 0.05). Modifications of FVC and diffusing capacity of the lungs for carbon monoxide (DLCO) over time were correlated with longitudinal radiological ILD modifications (r=-0.40, p < 0.01; r=-0.40, p < 0.01 respectively).</p><p><strong>Conclusion: </strong>AI-based automatic quantification of lesions from chest-CT images in SSc-ILD is correlated with physiological parameters and can help in disease evaluation. Further clinical multicentric validation is necessary in order to confirm its potential in the prediction of patient's outcome and in treatment management.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"39"},"PeriodicalIF":5.8,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11762107/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143041373","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Risk of lung disease with the Pi*SS genotype of alpha-1 antitrypsin: the evidence in context.","authors":"Helen O'Brien, Cormac McCarthy, Alessandro N Franciosi","doi":"10.1186/s12931-024-03066-9","DOIUrl":"10.1186/s12931-024-03066-9","url":null,"abstract":"","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"37"},"PeriodicalIF":5.8,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11763142/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143042225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Response to: risk of lung disease with the Pi*SS genotype of alpha-1 antitrypsin: the evidence in context.","authors":"Teresa Martín, Marc Miravitlles","doi":"10.1186/s12931-024-03065-w","DOIUrl":"10.1186/s12931-024-03065-w","url":null,"abstract":"","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"36"},"PeriodicalIF":5.8,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11762059/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143042141","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neutrophil extracellular traps (NETs) are increased in rheumatoid arthritis-associated interstitial lung disease.","authors":"Jing Xue, Miaomiao Nian, Yangyang Liang, Zeqin Zhu, Zhenyu Hu, Yuanyuan Jia, Shuhong Chi, Juan Chen","doi":"10.1186/s12931-025-03111-1","DOIUrl":"10.1186/s12931-025-03111-1","url":null,"abstract":"<p><strong>Background: </strong>Neutrophil extracellular trap (NET) formation has been implicated as a pathogenic mechanism in both rheumatoid arthritis (RA) and interstitial lung disease (ILD). However, the role of NETs in RA-associated ILD (RA-ILD) and the mechanisms driving NET formation remain unclear. This study aimed to assess the involvement of NETs in RA-ILD and elucidate the underlying mechanisms.</p><p><strong>Methods: </strong>Single-cell sequencing was used to identify changes in the quantity and function of neutrophils in the lung tissue of a zymosan A (ZYM)-induced interstitial pneumonia arthritis model. Additionally, nuclear receptor 4A3 (NR4A3) interference was performed in HL-60 cells to assess its impact on NET formation and the transformation of MRC-5 cells into myofibroblasts. The clinical relevance of plasma myeloperoxidase-DNA (MPO-DNA), citrullinated histone 3 (Cit-H3), and cell-free DNA was evaluated in RA-ILD patients with different imaging types via a commercial enzyme-linked immunosorbent assay (ELISA).</p><p><strong>Results: </strong>In the ZYM-treated SKG mouse model, which recapitulates key features of RA-ILD, an increased population of neutrophils in the lung tissue was primarily responsible for NET formation. Mechanistically, we found that interference with NR4A3 expression enhanced NET formation in HL-60 cells, which in turn promoted the differentiation of MRC-5 cells into myofibroblasts. Clinically, plasma MPO-DNA levels are elevated in patients with RA-nonspecific interstitial pneumonia (RA-NSIP), whereas Cit-H3 levels are elevated in RA-usual interstitial pneumonia (RA-UIP) patients compared with healthy subjects. ROC curve analysis further revealed that the combination of plasma MPO-DNA, rheumatoid factor (RF), and anti-citrullinated protein (anti-CCP) and the combination of Cit-H3, RF, and anti-CCP were superior diagnostic panels for NSIP and UIP in RA-ILD patients, respectively. Moreover, compared with those from healthy controls, neutrophils from patients with RA-UIP and RA-NSIP demonstrated a significantly increased ability to form NETs and induce the differentiation of MRC-5 cells into myofibroblasts. Specifically, RA-UIP patients exhibited a greater capacity for NET formation and the differentiation of MRC-5 cells into myofibroblasts than did RA-NSIP patients.</p><p><strong>Conclusions: </strong>These findings suggest that targeting NETs may be a novel therapeutic approach for treating ILD in RA patients.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"33"},"PeriodicalIF":5.8,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11756115/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143025342","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The fibronectin-targeting PEG-FUD imaging probe shows enhanced uptake during fibrogenesis in experimental lung fibrosis.","authors":"Thomas J Harr, Nikesh Gupta, Babita Rahar, Kristen Stott, Yadira Medina-Guevara, Metti K Gari, Angie T Oler, Ivy Sohee McDermott, Hye Jin Lee, Morteza Rasoulianboroujeni, Ashley M Weichmann, Amir Forati, Kelsey Holbert, Trevor S Langel, Kade W Coulter, Brian M Burkel, Bianca R Tomasini-Johansson, Suzanne M Ponik, Jonathan W Engle, Reinier Hernandez, Glen S Kwon, Nathan Sandbo, Ksenija Bernau","doi":"10.1186/s12931-025-03107-x","DOIUrl":"10.1186/s12931-025-03107-x","url":null,"abstract":"<p><p>Progressive forms of interstitial lung diseases, including idiopathic pulmonary fibrosis (IPF), are deadly disorders lacking non-invasive biomarkers for assessment of early disease activity, which presents a major obstacle in disease management. Excessive extracellular matrix (ECM) deposition is a hallmark of these disorders, with fibronectin being an abundant ECM glycoprotein that is highly upregulated in early fibrosis and serves as a scaffold for the deposition of other matrix proteins. Due to its role in active fibrosis, we are targeting fibronectin as a biomarker of early lung fibrosis disease activity via the PEGylated fibronectin-binding polypeptide (PEG-FUD). In this work, we demonstrate the binding of PEG-FUD to the fibrotic lung throughout the course of bleomycin-induced murine model of pulmonary fibrosis. We first analyzed the binding of radiolabeled PEG-FUD following direct incubation to precision cut lung slices from mice at different stages of experimental lung fibrosis. Then, we administered fluorescently labeled PEG-FUD subcutaneously to mice over the course of bleomycin-induced pulmonary fibrosis and assessed peptide uptake 24 h later through ex vivo tissue imaging. Using both methods, we found that peptide targeting to the fibrotic lung is increased during the fibrogenic phase of the single dose bleomycin lung fibrosis model (days 7 and 14 post-bleomycin). At these timepoints we found a correlative relationship between peptide uptake and fibrotic burden. These data suggest that PEG-FUD targets fibronectin associated with active fibrogenesis in this model, making it a promising candidate for a clinically translatable molecular imaging probe to non-invasively determine pulmonary fibrosis disease activity, enabling accelerated therapeutic decision-making.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"34"},"PeriodicalIF":5.8,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11756063/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143025348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extracellular matrix turnover in severe COVID-19 is reduced by corticosteroids.","authors":"Janesh Pillay, Antine W Flikweert, Matijs van Meurs, Marco J Grootenboers, Simone van der Sar-van der Brugge, Peter H J van der Voort, Morten A Karsdal, Jannie M B Sand, Diana J Leeming, Janette K Burgess, Jill Moser","doi":"10.1186/s12931-025-03098-9","DOIUrl":"10.1186/s12931-025-03098-9","url":null,"abstract":"<p><strong>Background: </strong>Severe and critical COVID-19 is characterized by pulmonary viral infection with SARS-CoV-2 resulting in local and systemic inflammation. Dexamethasone (DEX) has been shown to improve outcomes in critically ill patients; however, its effect on tissue remodeling, particularly collagen turnover, remains unclear. This study investigated the association between circulating extracellular matrix (ECM) remodeling neo-epitopes and COVID-19 severity, their relationship with mortality, and the effect of DEX on these markers.</p><p><strong>Methods: </strong>We conducted a multi-center prospective cohort study involving 226 COVID-19 patients: 157 with severe disease admitted to the ward and 69 with critical disease admitted to the ICU. Plasma samples were collected at ICU admission and at discharge or death. Circulating collagen degradation (C3M, C4Ma3, and C6M) and synthesis (PRO-C3, PRO-C4, and PRO-C6) neo-epitopes were measured. Longitudinal analysis of ECM neo-epitope changes during ICU stay and their association with mortality was performed, along with an evaluation of the impact of DEX treatment on these markers.</p><p><strong>Results: </strong>Critically ill patients exhibited higher levels of collagen degradation (reflecting inflammatory driven ECM destruction) (C3M, C6M) and collagen synthesis (strongly related to fibroblast activity) (PRO-C3, PRO-C6) neo-epitopes than severe patients. Increased collagen turnover, measured during ICU stay, was associated with mortality. Non-survivors displayed rising levels of collagen degradation and synthesis markers over time, whereas survivors had stable or declining levels. In non-survivors without DEX treatment, C6M and PRO-C6 levels were significantly increased, whereas these elevations were less pronounced in patients treated with DEX.</p><p><strong>Conclusion: </strong>Our findings suggest that elevated collagen turnover is associated with poor outcomes in critically ill COVID-19 patients. DEX treatment appeared to attenuate ECM remodeling, although this effect was not linked to improved survival. Further studies are needed to confirm these observations and better understand the role of ECM remodeling in COVID-19 and the potential therapeutic impact of corticosteroids.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"32"},"PeriodicalIF":5.8,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11755962/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143025255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}