EUROPEAN RESPIRATORY JOURNAL欧洲呼吸杂志
EUROPEAN RESPIRATORY JOURNAL(英文缩写 EUR RESPIR J),ISSN 0903-1936,eISSN 1399-3003,中文译名:欧洲呼吸杂志 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：2025-09-27 至 2026-09-27，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 | 33.801 | Q1 |
| 2022 | 24.300 | Q1 |
| 2023 | 16.600 | Q1 |
| 2024 | 21.000 | Q1 |
| 2025 | 23.800 | Q1 |
EUROPEAN RESPIRATORY JOURNAL 最新收录文献
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1. Preserved terminal bronchiole density in PAH revealed by micro-CT imaging.
PMID:日期:2026-09-24该文献暂无摘要。
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2. The regulatory landscape in tuberculosis integrated research platforms.
PMID:日期:2026-09-24Tuberculosis (TB) is the infectious disease with the highest mortality burden globally. Despite a recently enriched drug pipeline, there has been limited advance in improving its treatment. Integrated research platforms (IRPs) provide a novel research framework which, by hosting adaptive platform trials, can streamline the evaluation of several new TB regimens, whilst reducing costs. However, there is no clear, evidence-based guidance on the use of IRPs for regulatory drug development in TB. This consensus statement summarizes the discussion and recommendations produced during the European Union Patient centric clinical trial platforms (EU-PEARL) project. A multidisciplinary task force reviewed the literature regarding regulatory pathways for IRP with special focus on TB and identified current gaps and needs, which were discussed by an extended panel in two consultations. Here we summarise the output of this process and propose possible ways to advance in the implementation of such platforms. IRP coordinators are advised to seek an early contact with national regulators and supranational organisms, including regulatory collaboration initiatives. To ensure regulatory acceptance, IRP must prioritize careful design, including clear decision rules for phase transitions, and the development of surrogate makers. Furthermore, data leverage and stratification across groups could enhance IRP success. These efforts will not only strengthen the scientific validity of the IRP but also enhance its regulatory acceptability and impact on global TB treatment strategies.
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3. Elexacaftor/tezacaftor/ivacaftor improves CFTR function to near-normal levels in children with cystic fibrosis.
3. Elexacaftor/tezacaftor/ivacaftor使囊性纤维化患儿的CFTR功能改善至接近正常水平PMID:日期:2026-09-24The CFTR modulator therapy elexacaftor/tezacaftor/ivacaftor (ETI) improves CFTR function in adolescents and adults with cystic fibrosis (CF) carrying at least one allele to around 40% of median CFTR activity in non-CF controls. This partial restoration of CFTR function is associated with residual mucus dysfunction, airway infection and inflammation. In clinical trials, ETI led to a larger reduction of sweat chloride concentration in children compared to adolescents and adults with CF. However, the degree of correction of CFTR function by ETI in children with CF is currently unknown. Therefore, the aim of this study was to quantify restoration of CFTR function in children with CF aged 2 to 11 years and one or two alleles. This prospective observational multicenter study quantified restoration of CFTR function by intestinal current measurements (ICM) before and 4 months after initiation of ETI. Additionally, we performed a combined analysis of the effects of ETI in children and our previous study in adolescents and adults with CF. A total of 26 children with CF and at least one allele were enrolled in this study. ETI improved cAMP-induced chloride secretory response to a median of 89.5% (IQR, 51.4 to 125.3; p<0.001) and increased the total chloride secretory response to 99.2% (IQR, 66.3 to 144.3; p<0.001) of median CFTR activity in non-CF controls. Furthermore, we observed strong correlations of the cAMP response and the total chloride response with age (R=0.43 and R=0.53 respectively, both p<0.001). Our results show that treatment with ETI results in near-normal CFTR function measured in freshly obtained rectal biopsies in children with CF aged 2 to 11 years and at least one allele.
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5. Single-cell multi-omics show disruption of blood and airway T cells in pulmonary long COVID.
5. 单细胞多组学揭示肺部长新冠中血液和气道T细胞的紊乱PMID:日期:2026-09-24Approximately 10% of individuals who recover from COVID-19 experience residual respiratory symptoms impacting their quality of life, but the mechanisms behind pulmonary long COVID (PLC) are largely unknown. We characterized airway and circulating immune cells in patients with and without PLC. Participants were recruited and allocated into two groups: 1) PLC, defined by a St. George's Respiratory Questionnaire (SGRQ) total score of >10 at least three months following an acute SARS-CoV-2 infection with self-reported new or worsening symptoms, and 2) controls, defined by SGRQ ≤10 with or without a prior history of COVID. We performed research bronchoscopy and obtained bronchoalveolar lavage (BAL) in seven PLC patients and seven age- and sex-matched control subjects. Single-cell RNA sequencing (scRNAseq) was performed on the BAL cells. Peripheral blood mononuclear cells (PBMCs) were cryopreserved in 30 participants (17 PLC, 13 controls) for proteomic analysis. Serum was submitted for microarray detection of auto-IgG antibodies. We annotated 105 836 cells using scRNAseq and found that CD4 T cells were credibly increased in participants with PLC. scRNAseq revealed up-regulation of anti-viral pathways including those related to interferon signaling in T cells as well as antigen presenting cells. In PBMCs, T cells expressing both CD4 and CD8 were elevated in PLC participants. Autoantibodies targeting histone 2B and histone 3 were significantly increased in PLC participants (adj.p<0.05). PLC is associated with dysregulation of T cell mediated immunity, which may be related to autoimmunity. These cells represent potential novel therapeutic targets in patients suffering from PLC.
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7. Beyond Heritable PAH: Pulmonary Hypertension in Genetic Syndromes.
PMID:日期:2026-09-10Pulmonary hypertension (PH) may complicate a broad range of genetic syndromes beyond the established spectrum of heritable pulmonary arterial hypertension. Although these conditions are individually rare, together they represent an emerging field at the crossroads of developmental biology, vascular medicine, and precision genomics. In many cases, PH may be the presenting feature or may remain unrecognized because it occurs within complex multisystem disorders involving congenital heart disease, developmental lung abnormalities, parenchymal lung disease, vascular malformations, or extra-pulmonary manifestations. Recent advances in human genetics have expanded the spectrum of genes and syndromes associated with PH, including disorders involving altered lung and vascular development, dysregulated hypoxia signaling, smooth muscle dysfunction, chromosomal abnormalities, and syndromic vasculopathies.In this review, we summarize the main genetic syndromes associated with PH and discuss their underlying mechanisms, clinical phenotypes, diagnostic clues, and therapeutic implications. We paid particular attention to conditions that illustrate the marked heterogeneity of syndromic PH such as -related disorders, neurofibromatosis type 1, Noonan syndrome, Down syndrome, Alagille syndrome, Cantú syndrome, Chuvash polycythaemia, cobalamin C deficiency, multisystemic smooth muscle dysfunction syndrome, alveolar capillary dysplasia with misalignment of pulmonary veins, and Moya Moya syndrome.
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9. Prognostic implication of malignant pleural metastases in stage M1a non-small cell lung cancer in a real-world Dutch cohort receiving chemotherapy and/or immunotherapy.
PMID:日期:2026-09-07In the updated 9th TNM non-small cell lung cancer (NSCLC) staging edition, pleural and pulmonary metastases remain grouped within the M1a category, inferring similar prognostic implications. The aim was to evaluate the prognostic implication on overall survival (OS) of pleural contralateral pulmonary metastases in a stage M1a cohort, when treated with immune checkpoint inhibitors (ICI), chemotherapy, or chemo-ICI. Retrospective real-world data from the Netherlands Cancer Registry was used, including patients with M1a NSCLC that received systemic treatment between 2010-2022. The primary outcome was 2-year OS. 5632 patients were included: 2701 with contralateral lung metastases, 2590 with pleural metastases and 341 with both. Pleural metastases were more common in men (p=<0.001), in patients with worse performance score (p=<0.001) and in patients receiving mono-ICI (p=<0.001).Patients with contralateral lung metastases had a better 2-year OS (for chemo, ICI and chemo-ICI, this was 26.9% (95% CI 24.9-28.9), 49.5% (95% CI 43.4-55.2) and 40.4% (95% CI 36.5-44.2), respectively) than patients with pleural metastases (18.5% (95% CI 16.6-20.4), 41.6% (95% CI 36.6-46.5) and 28.6% (95% CI 24.9-32.4), respectively). Patients with both contralateral lung and pleural metastases had the worst OS (12.1% (95% CI 8.2-16.7), 31.1% (95% CI 18.4-44.7) and 25.0% (95% CI 15.7-35.4), respectively). The difference in OS was irrespective of the type of systemic treatment. Patients with pleural metastases have inferior OS compared to those with contralateral lung metastases. These findings indicate prognostic heterogeneity between M1a descriptors.
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10. Solving an enigma: the BMP-9/10 axis as a key regulator of pulmonary vascular resilience.
PMID:日期:2026-09-07The circulating ligands bone morphogenetic protein (BMP)-9 and BMP-10 are emerging as dual regulators of pulmonary and systemic vascular biology. Acting through activin receptor-like kinase 1 (ALK1), BMP receptor type II (BMPRII) and endoglin receptor complexes, they maintain endothelial quiescence and vascular tone under physiological conditions. Yet, the same axis can turn pathogenic when its intensity, timing or cellular context are altered. We propose viewing BMP-9/10 not as a linear protective pathway but as a bimodal system in which both deficiency and hyperactivation disrupt vascular homeostasis, leading to distinct phenotypes such as obstructive pulmonary arterial remodeling in pulmonary arterial hypertension (PAH), intrapulmonary vasodilatation in hepatopulmonary syndrome (HPS), and arteriovenous shunting in hereditary haemorrhagic telangiectasia (HHT). The clinical success of sotatercept, an activin signaling inhibitor with partial BMP-ligand trap properties, underscores the translational potential of therapeutically "retuning" this pathway rather than globally enhancing it. Understanding when BMP-9/10 signaling protects and when it becomes pathogenic will be crucial for designing next-generation interventions that stabilize, instead of destabilize, pulmonary vascular integrity.