
Respiratory Medicine, Journal Year: 2025, Volume and Issue: unknown, P. 107997 - 107997
Published: Feb. 1, 2025
Language: Английский
Respiratory Medicine, Journal Year: 2025, Volume and Issue: unknown, P. 107997 - 107997
Published: Feb. 1, 2025
Language: Английский
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
654American 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
338American 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
172Archivos de Bronconeumología, Journal Year: 2021, Volume and Issue: 58(1), P. 69 - 81
Published: March 18, 2021
Language: Английский
Citations
154Free 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
123Cell Death and Differentiation, Journal Year: 2023, Volume and Issue: 30(5), P. 1293 - 1304
Published: Feb. 24, 2023
Language: Английский
Citations
77Archivos de Bronconeumología, Journal Year: 2023, Volume and Issue: 59(4), P. 232 - 248
Published: March 1, 2023
Language: Английский
Citations
62Signal Transduction and Targeted Therapy, Journal Year: 2024, Volume and Issue: 9(1)
Published: Sept. 20, 2024
Language: Английский
Citations
37Gut, 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
17Journal 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