European Respiratory Review最新文献

{"title":"Impact of obstructive sleep apnoea on nocturnal blood pressure: mechanisms and treatment responses - a narrative review.","authors":"Bastian Gruber, Lara Benning, Zoe Bousraou, Dario Somaini, Esther Irene Schwarz","doi":"10.1183/16000617.0192-2026","DOIUrl":"10.1183/16000617.0192-2026","url":null,"abstract":"<p><p>Nocturnal blood pressure (BP) is a major determinant of cardiovascular risk. In obstructive sleep apnoea (OSA), abnormal nocturnal BP patterns, particularly nondipping and nocturnal hypertension, are common and contribute to excess cardiovascular risk. However, this association remains insufficiently integrated into routine clinical practice, as BP assessment still relies largely on office or home measurements and ambulatory BP monitoring is underused. This narrative review summarises current evidence on the physiological regulation of nocturnal BP, the mechanisms by which OSA disrupts nocturnal BP control, the epidemiology and prognostic relevance of abnormal nocturnal BP patterns in OSA, and the effects of available therapies. Continuous positive airway pressure (CPAP) has the strongest evidence base and lowers nocturnal BP modestly on average, with greater effects in patients with uncontrolled or resistant hypertension and with better treatment adherence. By contrast, evidence for non-CPAP therapies, including mandibular advancement devices, supplemental oxygen, hypoglossal nerve stimulation and upper-airway surgery, remains limited and less consistent. In summary, nocturnal BP abnormalities are common, clinically important and frequently overlooked in OSA. Greater use of ambulatory BP monitoring and more precise identification of patients most likely to benefit from targeted treatment may improve cardiovascular risk stratification and management in OSA.</p>","PeriodicalId":12166,"journal":{"name":"European Respiratory Review","volume":"35 181","pages":""},"PeriodicalIF":10.8,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13598623/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149029611","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Iron and the lung: emerging roles of iron metabolism in pulmonary disease pathogenesis and therapy.","authors":"Apostolos Galaris, Dimitrios Toumpanakis, Dimitrios Galaris, Theodoros Vassilakopoulos, Kostas Pantopoulos","doi":"10.1183/16000617.0160-2026","DOIUrl":"10.1183/16000617.0160-2026","url":null,"abstract":"<p><p>Iron is an essential micronutrient, but its redox reactivity also renders it potentially toxic. The lungs are particularly vulnerable to iron-dependent oxidative injury due to continuous exposure to high oxygen tension, environmental particles, and microbial pathogens. Pulmonary iron homeostasis is therefore tightly regulated at systemic, cellular, and local levels through coordinated actions of transferrin, ferritin, ferroportin, hepcidin, and the iron responsive element/iron regulatory protein system. Disruption of these pathways contributes to a broad spectrum of pulmonary diseases. In COPD, asthma, idiopathic pulmonary fibrosis, pulmonary arterial hypertension, infectious lung diseases, and lung cancer, iron dysregulation promotes oxidative stress, ferroptosis, inflammation, aberrant repair, vascular remodelling, or pathogen persistence. Notably, systemic iron deficiency may coexist with local pulmonary iron overload, highlighting the compartmentalised nature of lung iron metabolism. Emerging experimental and clinical evidence suggests that therapeutic manipulation of iron availability through supplementation, chelation or targeting iron-dependent pathways may be beneficial in selected contexts. A deeper mechanistic understanding and improved biomarkers will be essential for developing disease-specific iron-modulating strategies.</p>","PeriodicalId":12166,"journal":{"name":"European Respiratory Review","volume":"35 181","pages":""},"PeriodicalIF":10.8,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13598627/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149029650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Occlusive <i>versus</i> non-occlusive CPAP interfaces in neonatal respiratory care: a comparative review of efficacy and safety.","authors":"Aleksandra Hibner, Samantha Hietalati, Sandra Lawrynowicz Leibel","doi":"10.1183/16000617.0061-2026","DOIUrl":"10.1183/16000617.0061-2026","url":null,"abstract":"<p><strong>Background: </strong>Continuous positive airway pressure (CPAP) is first-line therapy for respiratory distress in preterm infants, but optimal interface selection remains controversial. Occlusive interfaces (nasal prongs and masks with tight seals) provide accurate pressure delivery but can cause significant nasal trauma, while non-occlusive interfaces (loosely fitting nasal cannulae) reduce trauma but may compromise therapeutic efficacy.</p><p><strong>Objective: </strong>To synthesise current evidence comparing occlusive with non-occlusive CPAP interfaces regarding pressure delivery accuracy, clinical efficacy, safety outcomes and practical implementation in neonatal intensive care.</p><p><strong>Methods: </strong>Comprehensive review of randomised controlled trials, systematic reviews, bench studies and observational studies comparing CPAP interface types in preterm neonates. Evidence quality assessed using the Grading of Recommendations Assessment, Development and Evaluation criteria where applicable.</p><p><strong>Results: </strong>Occlusive interfaces deliver pressure within 0.5-1.0 cmH₂O of set values and demonstrate superior efficacy in landmark trials (COIN, SUPPORT), particularly in extremely preterm infants (<28 weeks' gestation). However, nasal trauma rates reach 20-60%. Non-occlusive systems reduce trauma dramatically (0-5.4% injury rates) but consistently underdeliver pressure. Non-occlusive systems have failed to meet non-inferiority criteria in recent trials, with CPAP failure rates of 19.7% <i>versus</i> 17.3% for occlusive systems. This increased to failure rates >50% in extremely preterm infants.</p><p><strong>Conclusions: </strong>Current evidence supports occlusive CPAP as first-line therapy for moderate-to-severe respiratory distress in preterm neonates, particularly those of <32 weeks' gestation. Non-occlusive interfaces may be appropriate for stable infants, weaning support or apnoea of prematurity management. Adequately powered randomised trials stratified by gestational age and respiratory severity are urgently needed to define optimal interface selection strategies.</p>","PeriodicalId":12166,"journal":{"name":"European Respiratory Review","volume":"35 181","pages":""},"PeriodicalIF":10.8,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13598625/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149029618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Defective alveolar regeneration in emphysema: identifying dysfunctional cellular crosstalk and novel therapeutic opportunities for tissue repair.","authors":"Landy Paola Torre Flores, Philip J Jalink, Rocío Fuentes-Mateos, Michiel Erasmus, Merel E van Oorschot, Tji Gan, Roland Hoffmann, Jaap Jan Zwaginga, Corry-Anke Brandsma, Martijn Nawijn, Lin Chen, Nirmayi Homkar, Jai Prakash, Pieter S Hiemstra, Anne M Van der Does, Jeroen Leijten, Reinoud Gosens, Irene Heijink","doi":"10.1183/16000617.0090-2026","DOIUrl":"10.1183/16000617.0090-2026","url":null,"abstract":"<p><p>A key problem underlying COPD is the severe and irreversible lung tissue damage (emphysema) as consequence of hampered repair. Available therapies do not halt or reverse disease progression, and novel therapeutic strategies aimed at tissue repair are urgently awaited. To address this unmet need, ongoing research aims to provide insight into the cellular/molecular mechanisms underpinning defective lung repair in emphysema. Healthy lungs possess an intrinsic regenerative capacity based on alveolar epithelial progenitor cells that reside in their niche, which is composed of a supporting extracellular matrix, stromal cells and immune cells. While this stromal niche is vital for appropriate regenerative responses, emerging studies show that interactions within the stromal niche are defective in COPD, hampering alveolar repair. This review addresses the novel concept that restoring disrupted interactions within the diseased stromal niche may lead to repair of damaged lung tissue in COPD. The unavailability of successful strategies to achieve stromal health and support lung tissue repair may be due to an incomplete insight into the complex interactions within the alveolus. Moreover, inadequate delivery methods, with uncontrolled release and rapid clearance of regenerative compounds and therapeutic cells, contribute to the failed translation of novel findings into effective strategies. This review provides an overview of the current state of the field, including novel insights into the defective interactions that have been identified within the alveolar niche in COPD. Moreover, advanced models to study the alveolar niche and innovative strategies to therapeutically target this niche and restore stromal health in COPD are discussed.</p>","PeriodicalId":12166,"journal":{"name":"European Respiratory Review","volume":"35 181","pages":""},"PeriodicalIF":10.8,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13598616/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149030260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Small airways dysfunction: associated factors, clinical aspects and new perspectives.","authors":"Brice Touilloux, Antonio Cartellà, Christophe von Garnier, Claire Descombes, Kevin Nguyen, Adam Ogna, Laurève Chollet, Julien Vaucher, Alessio Casutt","doi":"10.1183/16000617.0008-2026","DOIUrl":"10.1183/16000617.0008-2026","url":null,"abstract":"<p><p>Scientific interest in small airways emerged in the 1960s. However, despite this early recognition, they long remained a \"silent\" area of the lung. In this nonsystematic narrative mini-review, we evaluated the different spirometry thresholds used to define small airways dysfunction (SAD), comparing them with other diagnostic techniques. We then examined the various factors associated with SAD, focusing on SAD as defined by spirometry.Maximal mid-expiratory flow, especially below the lower limit of normal (LLN), appears to be the most accurate and reproducible spirometric measure to assess SAD. However, no gold-standard spirometric definition has been endorsed by respiratory academic societies, and forced expiratory volume in 3 s or 6 s <LLN or combined forced expiratory flow could be alternative criteria. Impulse oscillometry or computed tomography scanning represent possible alternative assessment methods, with limitations regarding reproducibility.Globally, prevalence of SAD varies between regions. Air pollution appears to be associated with a higher prevalence of SAD, particularly particulate matter with aerodynamic diameter <2.5 µm. Both active and passive smoking are associated with SAD. SAD is also strongly associated with COPD and the risk of developing it, making SAD a marker of accelerated decline in lung function. Several occupational exposures are associated with SAD, including exposure to organic and inorganic dust. A history of lung infections, especially tuberculosis, is also associated with SAD. Advanced age may also be an associated factor, although the association depends on the criteria used to define SAD. Cardiac events have been associated to SAD, which might explain the association between SAD and higher mortality risk.By integrating these different associations in clinical assessment, it would be possible to screen more reliably and preventively for SAD. This would ensure closer surveillance, which is justified given the strong association with COPD.</p>","PeriodicalId":12166,"journal":{"name":"European Respiratory Review","volume":"35 181","pages":""},"PeriodicalIF":10.8,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13598626/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149029727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comorbidities in clinical cohorts of patients with idiopathic pulmonary fibrosis: a systematic review and meta-analysis.","authors":"Marcus C H Leong, Seema Green, Mingkun Guan, Tyson M Walters, Emma Marshall, Chunbouy Sok, Nicole S L Goh, Christopher J Ryerson, Yet H Khor","doi":"10.1183/16000617.0098-2026","DOIUrl":"10.1183/16000617.0098-2026","url":null,"abstract":"<p><strong>Background: </strong>Comorbidities can influence treatment decisions and health outcomes in patients with idiopathic pulmonary fibrosis (IPF). This systematic review and meta-analysis evaluated the types and prevalence of comorbidities, as well as their impact on health outcomes, in clinical cohorts of patients with IPF.</p><p><strong>Methods: </strong>Ovid MEDLINE and Embase were searched up to August 2024 for eligible observational studies with ≥100 adults with IPF that reported at least one comorbidity. Meta-analyses were performed for comorbidity prevalence, with associations between comorbidities and health outcomes narratively synthesised.</p><p><strong>Results: </strong>A total of 251 studies (n=606 398 participants) were included. Common comorbidities were systemic hypertension (pooled prevalence 39%, 95% confidence interval (CI) 34-44%), dyslipidaemia (30%, 95% CI 20-38%), gastro-oesophageal reflux disease (27%, 95% CI 23-31%), hiatus hernia (20%, 95% CI 9-33%), overweight/obesity (22%, 95% CI 18-27%), diabetes mellitus (21%, 95% CI 19-23%), ischaemic heart disease (20%, 95% CI 17-23%) and heart failure (15%, 95% CI 13-18%). Few studies evaluated the relationships between comorbidities and health-related quality of life or IPF disease progression. Lung cancer was the only comorbidity that was consistently associated with increased short-term and long-term mortality in patients with IPF.</p><p><strong>Conclusions: </strong>A wide variety of comorbidities affect clinically encountered patients with IPF, with many having higher prevalence rates than those reported in clinical trial cohorts. This highlights the need for personalised care in the management of IPF. The relationships between different comorbidities and health outcomes warrant future studies to better inform targeted screening and management.</p>","PeriodicalId":12166,"journal":{"name":"European Respiratory Review","volume":"35 181","pages":""},"PeriodicalIF":10.8,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13555312/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148918618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Normal age-related decline in forced vital capacity: a systematic review and meta-analysis.","authors":"Imran Satia, Katlyn Brown, Jody Filkowski, Glenda Babe, Raymond Milan, Sean Tiggelaar, Martin Kolb","doi":"10.1183/16000617.0329-2025","DOIUrl":"10.1183/16000617.0329-2025","url":null,"abstract":"<p><p>Lung function peaks in early adulthood and declines thereafter, even without respiratory disease. Differentiating physiological ageing from pathological trajectories is critical for diagnosis, prognostication and interpretation of clinical trial end-points, particularly in interstitial lung diseases where attenuation of forced vital capacity (FVC) decline is a primary outcome in most trials. Without a benchmark for expected ageing, it is difficult to determine whether therapy preserves lung function by preventing FVC loss or mirrors natural trajectories. We conducted a systematic review and meta-analysis of longitudinal evidence on age-related FVC changes among adults without lung disease. A search of major databases and conference proceedings identified 7160 citations; 50 publications representing 35 cohorts and over 365 000 participants met eligibility criteria. Follow-up ranged from three to 35 years, with three to 12 spirometric assessments per participant. Over five decades of research, a consistent pattern of decline after early adulthood was evident, but estimates varied widely (10-80 mL·year^-1) due to heterogeneity in study design, population composition, outcome reporting and analytic approach. The strongest evidence came from an individual-level pooled analysis of over 30 000 participants, demonstrating that FVC peaks in the mid-20s, declines continuously without plateau and follows a linear trajectory in women (∼26 mL·year^-1) and a biphasic trajectory in men (∼22 mL·year^-1 before age 40, ∼36 mL·year^-1 thereafter). These normative trajectories, averaging ∼20-30 mL annually, are essential for distinguishing healthy ageing from pathological decline. Incorporating these into clinical practice and trial design will improve diagnostic precision, contextualise therapeutic effects and define clinically meaningful preservation of lung function.</p>","PeriodicalId":12166,"journal":{"name":"European Respiratory Review","volume":"35 181","pages":""},"PeriodicalIF":10.8,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13555310/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148918815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"\"Ventilator-induced diaphragmatic dysfunction: pathophysiology, monitoring and advances in potential treatment and prevention.\" W. Fu, L. Guan, Q. Liu <i>et al</i>. <i>Eur Respir Rev</i> 2025; 34: 250069.","authors":"","doi":"10.1183/16000617.5069-2025","DOIUrl":"10.1183/16000617.5069-2025","url":null,"abstract":"","PeriodicalId":12166,"journal":{"name":"European Respiratory Review","volume":"35 181","pages":""},"PeriodicalIF":10.8,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13555301/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148918547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Frailty and COPD: a bidirectional relationship in the context of systemic and accelerated ageing.","authors":"Mauro Maniscalco, Claudio Candia, Salvatore Fuschillo, Pasquale Ambrosino, Klara Komici, Giuseppe Rengo","doi":"10.1183/16000617.0340-2025","DOIUrl":"10.1183/16000617.0340-2025","url":null,"abstract":"<p><p>Chronic obstructive pulmonary disease (COPD) is increasingly recognised as a systemic disorder that extends beyond the lungs, representing a clinical model of accelerated ageing. Frailty, a multidimensional syndrome characterised by reduced physiological reserve and increased vulnerability to stressors, is highly prevalent among individuals with COPD and contributes to adverse outcomes. Both conditions share common biological mechanisms, including chronic inflammation, oxidative stress, endocrine dysregulation, mitochondrial dysfunction and skeletal muscle atrophy. Exercise acts as a physiological stressor that elicits hormetic responses, triggering favourable molecular adaptations such as enhanced mitochondrial biogenesis, improved redox balance and the upregulation of antioxidant and cellular repair pathways. These adaptations translate into improved muscle function, metabolic efficiency and immune homeostasis, thereby counteracting the catabolic processes that underlie both frailty and COPD progression. Scientific evidence supports the role of combined aerobic, resistance and balance training as the most effective approach to improving functional status and quality of life in frail individuals with COPD. Frailty in COPD represents a potentially reversible state of systemic vulnerability rooted in accelerated biological ageing. Exercise thus constitutes a powerful, multi-target intervention capable of reprogramming molecular ageing pathways and promoting resilience across organ systems. Integrating exercise physiology with the principles of geroscience offers a promising framework for personalised rehabilitation strategies aimed at extending health span in patients with COPD. This narrative review summarises current evidence on the biological and clinical interplay between COPD, frailty and exercise, exploring how physical activity exerts systemic anti-ageing effects through modulation of inflammation, oxidative stress, mitochondrial and myokine signalling, ultimately restoring physiological resilience.</p>","PeriodicalId":12166,"journal":{"name":"European Respiratory Review","volume":"35 181","pages":""},"PeriodicalIF":10.8,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13555319/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148918776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The future of home oxygen therapy.","authors":"Anne E Holland, Jerry A Krishnan, Yves Lacasse, Humberto Gomes, Filip Björklund, Richard Casaburi, Joao de Andrade, Michelle N Eakin, David Hui, Susan S Jacobs, Shohei Kawachi, Yet H Khor, François Maltais, Christine F McDonald, Hugh Musick, Chris Ryerson, Magnus Ekström","doi":"10.1183/16000617.0144-2026","DOIUrl":"https://doi.org/10.1183/16000617.0144-2026","url":null,"abstract":"<p><p>Home oxygen therapy is a well-accepted treatment for advanced respiratory disease; however, there are substantial evidence gaps and implementation challenges. The patient experience varies widely; oxygen therapy devices are often poorly matched to patient needs; and adherence is suboptimal. Recent clinical trials have failed to demonstrate positive outcomes of home oxygen therapy across a range of indications and patient groups, raising new questions regarding which patients will benefit. We convened a home oxygen therapy summit, bringing together experts in the fields of hypoxia biology, biomarkers, home oxygen therapy, behavioural science, and clinical trials, to identify the critical steps necessary to advance the science and practice of home oxygen therapy. Prescription of oxygen therapy depends on identification of hypoxaemia, with or without evidence of end-organ dysfunction. However, this does not acknowledge that hypoxaemia does not always yield hypoxia, and ignores adaptation to hypoxia. There is a pressing need for a hypoxia biomarker that is sensitive and specific, reflects the mechanisms of adaptation and maladaptation to chronic hypoxia, and is responsive to change with supplemental oxygen. Advances in research and clinical care will require more \"usable\" devices that meet the needs of patients and provide value for payers. Optimising oxygen devices will require new technologies with greater portability and greater capacity for oxygen delivery. Registry-based clinical trials may allow measurement of long-term outcomes and identification of patients most likely to benefit from oxygen therapy. Collaborations between patients, clinicians, researchers, payers and industry will be critical to drive this field forward.</p>","PeriodicalId":12166,"journal":{"name":"European Respiratory Review","volume":"35 181","pages":""},"PeriodicalIF":10.8,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13482683/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148790092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}