European Respiratory Review欧洲呼吸评论
European Respiratory Review(英文缩写 EUR RESPIR REV),ISSN 0905-9180,eISSN 1600-0617,中文译名:欧洲呼吸评论 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 9.553 | Q1 |
| 2022 | 7.500 | Q1 |
| 2023 | 9.000 | Q1 |
| 2024 | 10.400 | Q1 |
| 2025 | 10.800 | Q1 |
European Respiratory Review 最新收录文献
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1. Maternal and fetal outcomes associated with CFTR modulator use during pregnancy: a scoping review.
PMID:日期:2026-09-23With major therapeutic advances driven by cystic fibrosis transmembrane conductance regulator (CFTR) modulators (CFTRm), increasing numbers of women with cystic fibrosis (CF) are living into adulthood and pursuing pregnancy. Women with CF may face pregnancy-related challenges that influence maternal and fetal outcomes. However, long-term data regarding the safety and effectiveness of CFTRm use during pregnancy remain limited.This scoping review aimed to evaluate the existing literature on the effects of CFTRm use in women with CF during pregnancy and the postpartum period, as well as the potential impact on the developing fetus. We analysed clinical studies, registry data and related literature published between 2003 and 2025 to assess reported differences in lung function, birth weight, pregnancy and neonatal complications, mode of delivery and screening biomarkers among pregnancies in women with CF treated with ivacaftor, lumacaftor/ivacaftor, tezacaftor/ivacaftor or elexacaftor/tezacaftor/ivacaftor, compared with pregnancies not exposed to CFTRm.Available evidence suggests that elexacaftor/tezacaftor/ivacaftor may improve maternal health through better lung function and nutritional status, while inadvertent fetal drug exposure has not been clearly associated with serious adverse outcomes. Reported fetal and neonatal outcomes following maternal CFTRm therapy have generally been reassuring. However, long-term effects in exposed children remain uncertain. There is also insufficient evidence to establish the safety of infant exposure or prolonged maternal CFTRm use during lactation. This review highlights the need for future studies evaluating dose optimisation, long-term follow-up of infants and children, and integration of registry data to better define the safety and effectiveness of CFTRm use during pregnancy.
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2. Iron and the lung: emerging roles of iron metabolism in pulmonary disease pathogenesis and therapy.
2. 铁与肺：铁代谢在肺部疾病发病机制和治疗中的新兴作用PMID:日期:2026-09-23Iron 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.
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3. Impact of obstructive sleep apnoea on nocturnal blood pressure: mechanisms and treatment responses - a narrative review.
PMID:日期:2026-09-23Nocturnal 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.
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4. Thymic neuroendocrine tumours: molecular landscape, immune microenvironment and therapeutic perspectives.
PMID:日期:2026-09-23Thymic neuroendocrine tumours (T-NETs) are rare, aggressive malignancies with distinct biology and poor outcomes. Current management is extrapolated from other neuroendocrine tumours (NETs), highlighting a critical need for a synthesised understanding of their unique molecular and immune landscape. We conducted a comprehensive narrative review (2000-2026) of T-NETs, interrogating PubMed, Embase, Web of Science and Scopus. Focus was placed on clinicopathology, molecular alterations, tumour immune microenvironment and therapeutic outcomes. T-NETs encompass a spectrum from well-differentiated carcinoids to high-grade carcinomas. Their molecular drivers are grade-specific, featuring TP53 (tumour protein p53)/RB1 (retinoblastoma 1) loss and chromosomal instability in high-grade tumours, alongside prevalent chromatin remodelling and PI3K (phosphatidylinositol 3-kinase)-mTOR (mechanistic target of rapamycin) dysregulation. The immune microenvironment is predominantly "inflamed", with heterogeneous PD-L1 (programmed death-ligand 1)/VISTA (V-domain Ig suppressor of T-cell activation) expression and T-cell infiltration that is often restrained by a myeloid-rich stroma. For clinical management, surgical resection is curative for localised disease. In advanced stages, therapy is extrapolated from other NETs and includes somatostatin analogues (for somatostatin receptor-positive tumours), everolimus, temozolomide-based regimens and, in selected cases, peptide receptor radionuclide therapy. Immunotherapy and novel combinations represent emerging investigational avenues. T-NETs are biologically distinct thymic malignancies. Improved care will require thymus-specific molecular and immune profiling, standardised diagnostic criteria, and prospective collaborative studies to move beyond extrapolated treatment paradigms.
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5. The gut-lung axis in early life: microbiome-associated mechanisms and clinical relevance.
PMID:日期:2026-09-23The early-life microbiome is increasingly recognised as a contributor to immune maturation and respiratory health. Early-life microbial colonisation is highly dynamic and shaped by multiple factors. Recently, the gut-lung axis has emerged as a framework describing bidirectional communication between the intestinal microbiota and the respiratory system microbial metabolites, immune mediators and neuroimmune pathways. Although current evidence is largely derived from studies of bacterial communities, emerging data suggest that other microbial components, including fungi and viruses, may also contribute to gut-lung interactions. This review synthesises current mechanistic and clinical evidence on the gut-lung axis with a specific focus on neonatology. We discuss how early microbiome composition may influence immune regulation, lung development and inflammatory response. Associations between intestinal microbiota alterations and major neonatal morbidities, including bronchopulmonary dysplasia, are discussed, as well as emerging evidence linking early-life microbial imbalance to long-term respiratory outcomes such as recurrent infections and asthma. We further examine emerging translational opportunities, including microbiome- and metabolome-based biomarkers for early risk stratification, and microbiota-targeted interventions. Attention is given to the strengths and limitations of the current evidence base, including the predominance of observational human studies and preclinical animal models. Overall, available evidence suggests that the developing microbiome represents a potentially important mediator of gut-lung communication in early life. However, substantial gaps remain regarding causality, underlying mechanisms and clinical applicability. Further longitudinal and interventional studies are needed to define the role of microbiome-targeted strategies in improving neonatal and long-term respiratory outcomes.
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6. Right ventricular-protective ventilation in acute respiratory distress syndrome: phenotypes, monitoring and ventilatory management.
PMID:日期:2026-09-23Despite the widespread implementation of lung-protective ventilation, mortality in acute respiratory distress syndrome (ARDS) remains substantial, underscoring the importance of extrapulmonary determinants of outcome. Right ventricular (RV) dysfunction is recognised as a frequent and clinically meaningful complication of ARDS, affecting a sizeable proportion of patients and consistently associated with adverse outcomes. ARDS-related pulmonary vascular injury, including hypoxic pulmonary vasoconstriction, hypercapnia and acidosis, microangiopathy, and an imbalance in vasoconstrictor/vasodilator signalling, reduces the functional pulmonary vascular bed and increases pulmonary vascular resistance, thereby imposing an acute afterload challenge on the thin-walled right ventricle. Mechanical ventilation may further exacerbate RV stress through alveolar overdistension, increased intrathoracic pressure and decreased venous return, promoting RV dilation, RV-pulmonary arterial uncoupling and circulatory collapse in severe cases. In this review, we summarise the pathophysiological basis of RV injury in ARDS and propose a physiology-informed clinical framework integrating RV phenotyping with multimodal monitoring. This includes echocardiography as the bedside cornerstone, selected invasive haemodynamic assessments and emerging noninvasive techniques such as electrical impedance tomography, as well as advanced cardiac imaging modalities and serological biomarkers for complementary assessment. We further discuss key components of RV-protective ventilation, including limitation of tidal volume and airway pressures, haemodynamics and recruitability-guided positive end-expiratory pressure titration, cautious use of permissive hypercapnia, avoidance of excessive mean airway pressure, prone positioning, appropriate application of spontaneous breathing and extracorporeal support to facilitate ultra-protective lung ventilation. Finally, we highlight unresolved clinical questions and emphasise the need for prospective studies incorporating standardised RV phenotypes and RV-centred end-points.
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7. Defective alveolar regeneration in emphysema: identifying dysfunctional cellular crosstalk and novel therapeutic opportunities for tissue repair.
7. 肺气肿中肺泡再生缺陷：识别功能失调的细胞串扰及组织修复的新治疗机会PMID:日期:2026-09-23A 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.
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8. Small airways dysfunction: associated factors, clinical aspects and new perspectives.
PMID:日期:2026-09-23Scientific 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.
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9. {"_":"Occlusive non-occlusive CPAP interfaces in neonatal respiratory care: a comparative review of efficacy and safety.","i":["versus"]}
PMID:日期:2026-09-23Continuous 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. 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. 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. Occlusive interfaces deliver pressure within 0.5-1.0 cmHO 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% 17.3% for occlusive systems. This increased to failure rates >50% in extremely preterm infants. 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.
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10. Pulmonary arterial hypertension with signs of venous/capillary involvement in connective tissue diseases: paradigms and paradoxes.
10. 结缔组织病中伴有静脉/毛细血管受累征象的肺动脉高压：范式与悖论PMID:日期:2026-09-23Pulmonary arterial hypertension (PAH) with features of venous and/or capillary involvement, formerly pulmonary veno-occlusive disease (PVOD), represents a rare and severe subset of pulmonary hypertension. While PVOD is typically idiopathic, heritable or drug/toxin-induced, "PVOD-like" features have long been recognised in PAH associated with connective tissue diseases (CTDs), especially systemic sclerosis (SSc). This review synthesises the available evidence on this phenotype, integrating published data with an unreported cohort of 25 patients. Venular remodelling is a frequent histological finding in SSc-PAH lung explants, but high-resolution computed tomography (HRCT) signs of PVOD are inconsistently observed at PAH presentation, reflecting a progression of the lung vasculopathy and/or an unmasking effect of pulmonary vasodilators. Patients often exhibit major functional limitation, profound impairment in gas transfer and severe haemodynamic compromise. Assessing venular involvement in SSc-PAH poses unique challenges, due to possible lung fibrosis on HRCT and differential diagnosis with an occult post-capillary component. Despite the lack of robust evidence, PAH-approved therapies are commonly used, although with caution due to a high risk of pulmonary oedema with pulmonary vasodilators. As these patients also display significant arteriolar involvement, which can benefit from these drugs, dedicated treatment strategies warrant further investigation. Prognosis remains dismal, with a 5-year survival around 45-50%. Similar PVOD-like patterns have also anecdotally been reported in systemic lupus erythematosus, rheumatoid arthritis, mixed connective tissue disease, Sjögren syndrome and inflammatory myopathies, with comparable features. Overall, PVOD-like disease in CTD-PAH constitutes a high-risk phenotype with unresolved pathogenic and management challenges, requiring refined patient stratification and improved therapeutic strategies.