Effect of traditional Chinese exercise on pulmonary function in middle-aged and older patients with stable chronic obstructive pulmonary disease: A randomized controlled trial DOI Creative Commons
Ziying Chen, Hongyu Yue, Yuanjia Gu

et al.

Respiratory Medicine, Journal Year: 2025, Volume and Issue: unknown, P. 107997 - 107997

Published: Feb. 1, 2025

Language: Английский

Global Initiative for Chronic Obstructive Lung Disease 2023 Report: GOLD Executive Summary DOI Creative Commons
Àlvar Agustí, Bartolomé R. Celli, Gerard J. Criner

et al.

European Respiratory Journal, Journal Year: 2023, Volume and Issue: 61(4), P. 2300239 - 2300239

Published: March 1, 2023

Executive summary of the Global Strategy for Prevention, Diagnosis and Management COPD 2023: latest evidence-based strategy document from Initiative Chronic Obstructive Lung Disease (GOLD) https://bit.ly/3KCaTGe

Language: Английский

Citations

654

Global Initiative for Chronic Obstructive Lung Disease 2023 Report: GOLD Executive Summary DOI Creative Commons
Àlvar Agustí, Bartolomé R. Celli, Gerard J. Criner

et al.

American Journal of Respiratory and Critical Care Medicine, Journal Year: 2023, Volume and Issue: 207(7), P. 819 - 837

Published: March 1, 2023

Language: Английский

Citations

338

From GOLD 0 to Pre-COPD DOI Creative Commons
MeiLan K. Han, Àlvar Agustí, Bartolomé R. Celli

et al.

American Journal of Respiratory and Critical Care Medicine, Journal Year: 2020, Volume and Issue: 203(4), P. 414 - 423

Published: Nov. 19, 2020

Currently the diagnosis of chronic obstructive pulmonary disease (COPD) requires demonstration airflow limitation, defined as a post-bronchodilator FEV 1 /FVC <0.7, measurement that remains methodologically robust and widely available.FEV is one most powerful predictors clinically relevant outcomes including symptoms, exacerbations mortality.However, reliable data suggest respiratory in particular bronchitis, airway abnormality emphysema detected using modern imaging techniques such computed tomography (CT), certain physiologic measures rapid decline DLCO are present among individuals who do not meet spirometric criteria for COPD.These abnormalities may help to identify at increased risk developing limitation future.Here, we review evidence support use term "pre-COPD" with symptoms (e.g., "Non-Obstructive Chronic Bronchitis" (NOCB)), low DLCO) and/or (e.g.CT emphysema) but spirometry normal range, COPD by reduced ratio.We acknowledge, however, further research on early young will be critical develop operable definition demonstrates good sensitivity specificity.

Language: Английский

Citations

172

Actualización 2021 de la Guía Española de la EPOC (GesEPOC). Tratamiento farmacológico de la EPOC estable DOI
Marc Miravitlles, Myriam Calle, Jesús Molina

et al.

Archivos de Bronconeumología, Journal Year: 2021, Volume and Issue: 58(1), P. 69 - 81

Published: March 18, 2021

Language: Английский

Citations

154

Hydrogen sulfide alleviates particulate matter-induced emphysema and airway inflammation by suppressing ferroptosis DOI Creative Commons
Ying Wang,

Sha Liao,

Zihan Pan

et al.

Free Radical Biology and Medicine, Journal Year: 2022, Volume and Issue: 186, P. 1 - 16

Published: April 29, 2022

Redox imbalance is an vital mechanism for COPD. At present, insufficient researches have been conducted on the protective effect of hydrogen sulfide (H2S) PM-induced However, whether H2S exerts anti-injury role by blocking ferroptosis and restoring redox equilibrium remain to be investigated. Human lung tissue samples were collected IHC staining, expressions Nrf2, ferritinophagy- ferroptosis-related proteins observed. The WT C57BL/6 Nrf2 knockout mice models established with PM(200 μg per mouse). NaHS(Exogenous H2S) was injected intraperitoneally 30 min in advance. Twenty-nine days later, tissues evaluated HE's PERLS-DAB's staining. Meanwhile, inflammation oxidative stress indicators iron levels assessed corresponding ELISA kit. Related protein detected through Western blot. BEAS-2B cells or without exposed PM2.5 36 h. Cell viability, mitochondrial morphology, inflammatory cytokines, antioxidant factors, levels, autophagic flux ROS, LIP MitoROS, MMP, as well related specific methods, respectively. In addition, V5-Nrf2, siRNA, inhibitor ML385, PPAR-γ GW9662, autophagy CQ, chelator DFO Fer-1 used verify target signaling pathways. We found that COX2, MDA other factors increased, while markers GPX4, GSH GSH-Px significantly decreased, active accumulation COPD patients, PM-exposured Nrf2-KO PM2.5-mediated cell models. NaHS pretreatment markedly inhibited emphysema airway alleviating ferroptotic changes vivo vitro. With use V5-Nrf2 overexpression plasmid, siRNA pathway inhibitors, we activates PPAR-γ, inhibites ferritinophagy makers LC3B, NCOA4 FTH1 cells. Moreover, anti-ferroptotic further verified activation signal MEF This research suggested alleviated via balance inhibiting regulating Nrf2-PPAR-ferritinophagy pathway.

Language: Английский

Citations

123

N6-Methyladenosine-modified circSAV1 triggers ferroptosis in COPD through recruiting YTHDF1 to facilitate the translation of IREB2 DOI
Haibo Xia,

Yan Wu,

Jing Zhao

et al.

Cell Death and Differentiation, Journal Year: 2023, Volume and Issue: 30(5), P. 1293 - 1304

Published: Feb. 24, 2023

Language: Английский

Citations

77

Global Initiative for Chronic Obstructive Lung Disease 2023 Report: GOLD Executive Summary DOI Creative Commons
Àlvar Agustí, Bartolomé R. Celli, Gerard J. Criner

et al.

Archivos de Bronconeumología, Journal Year: 2023, Volume and Issue: 59(4), P. 232 - 248

Published: March 1, 2023

Language: Английский

Citations

62

Pyroptosis in health and disease: mechanisms, regulation and clinical perspective DOI Creative Commons
Yifan Liu,

Renjie Pan,

Yuzhen Ouyang

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2024, Volume and Issue: 9(1)

Published: Sept. 20, 2024

Language: Английский

Citations

37

Faecal microbial transfer and complex carbohydrates mediate protection against COPD DOI Creative Commons
Kurtis F. Budden, Shakti D. Shukla, Kate L Bowerman

et al.

Gut, Journal Year: 2024, Volume and Issue: 73(5), P. 751 - 769

Published: Feb. 8, 2024

Objective Chronic obstructive pulmonary disease (COPD) is a major cause of global illness and death, most commonly caused by cigarette smoke. The mechanisms pathogenesis remain poorly understood, limiting the development effective therapies. gastrointestinal microbiome has been implicated in chronic lung diseases via gut-lung axis, but its role unclear. Design Using an vivo mouse model smoke (CS)-induced COPD faecal microbial transfer (FMT), we characterised microbiota using metagenomics, proteomics metabolomics. Findings were correlated with airway systemic inflammation, gut histopathology function. Complex carbohydrates assessed mice high resistant starch diet, 16 patients randomised, double-blind, placebo-controlled pilot study inulin supplementation. Results FMT alleviated hallmark features (inflammation, alveolar destruction, impaired function), pathology immune changes. Protective effects additive to smoking cessation, CS-associated after antibiotic-induced depletion was sufficient increase inflammation while suppressing colonic immunity absence CS exposure. Disease relative abundance Muribaculaceae, Desulfovibrionaceae Lachnospiraceae family members. Proteomics metabolomics identified downregulation glucose metabolism microbiota, supplementation or human complex improved outcomes. Conclusion contributes can be targeted therapeutically.

Language: Английский

Citations

17

Chronic Obstructive Pulmonary Disease: Epidemiology, Biomarkers, and Paving the Way to Lung Cancer DOI Open Access

Klára Szalontai,

Nikolett Gémes, József Furák

et al.

Journal of Clinical Medicine, Journal Year: 2021, Volume and Issue: 10(13), P. 2889 - 2889

Published: June 29, 2021

Chronic obstructive pulmonary disease (COPD), the frequently fatal pathology of respiratory tract, accounts for half a billion cases globally. COPD manifests via chronic inflammatory response to irritants, tobacco smoke. The progression from early onset advanced leads loss alveolar wall, hypertension, and fibrosis epithelium. Here, we focus on epidemiology, progression, biomarkers with particular connection lung cancer. Dissecting cellular molecular players in disease, aim shed light role smoking, which is responsible or at least more severe symptoms worse patient outcomes. We summarize conditions, as well EMT fibroblasts establishing cancer-prone microenvironment, i.e., soil 'COPD-derived' highlight that major health problem can be alleviated smoking cessation, diagnosis, abandonment usage biomass fuels global basis.

Language: Английский

Citations

86