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International Journal of Chronic... 2023The comorbidity of pulmonary fibrosis and COPD/emphysema has garnered increasing attention. However, no bibliometric analysis of this comorbidity has been conducted thus...
OBJECTIVE
The comorbidity of pulmonary fibrosis and COPD/emphysema has garnered increasing attention. However, no bibliometric analysis of this comorbidity has been conducted thus far. This study aims to perform a bibliometric analysis to explore the current status and cutting-edge trends in the field, and to establish new directions for future research.
METHODS
Statistical computing, graphics, and data visualization tools such as VOSviewer, CiteSpace, Biblimatrix, and WPS Office were employed.
RESULTS
We identified a total of 1827 original articles and reviews on the comorbidity of pulmonary fibrosis and COPD/emphysema published between 2004 and 2023. There was an observed increasing trend in publications related to this comorbidity. The United States, Japan, and the United Kingdom were the countries with the highest contributions. Professor Athol Wells and the University of Groningen had the highest h-index and the most articles, respectively. Through cluster analysis of co-cited documents, we identified the top 17 major clusters. Keyword analysis predicted that NF-κB, oxidative stress, physical activity, and air pollution might be hot spots in this field in the future.
CONCLUSION
This bibliometric analysis demonstrates a continuous increasing trend in literature related to the comorbidity of pulmonary fibrosis and COPD/emphysema. The research hotspots and trends identified in this study provide a reference for in-depth research in this field, aiming to promote the development of the comorbidity of pulmonary fibrosis and COPD/emphysema.
Topics: Humans; Pulmonary Fibrosis; Pulmonary Disease, Chronic Obstructive; Comorbidity; Emphysema; Pulmonary Emphysema
PubMed: 37720874
DOI: 10.2147/COPD.S426763 -
Frontiers in Public Health 2023Long COVID is a clinical entity characterized by persistent health problems or development of new diseases, without an alternative diagnosis, following SARS-CoV-2...
BACKGROUND
Long COVID is a clinical entity characterized by persistent health problems or development of new diseases, without an alternative diagnosis, following SARS-CoV-2 infection that affects a significant proportion of individuals globally. It can manifest with a wide range of symptoms due to dysfunction of multiple organ systems including but not limited to cardiovascular, hematologic, neurological, gastrointestinal, and renal organs, revealed by observational studies. However, a causal association between the genetic predisposition to COVID-19 and many post-infective abnormalities in long COVID remain unclear.
METHODS
Here we employed Mendelian randomization (MR), a robust genetic epidemiological approach, to investigate the potential causal associations between genetic predisposition to COVID-19 and long COVID symptoms, namely pulmonary (pneumonia and airway infections including bronchitis, emphysema, asthma, and rhinitis), neurological (headache, depression, and Parkinson's disease), cardiac (heart failure and chest pain) diseases, and chronic fatigue. Using two-sample MR, we leveraged genetic data from a large COVID-19 genome-wide association study and various disorder-specific datasets.
RESULTS
This analysis revealed that a genetic predisposition to COVID-19 was significantly causally linked to an increased risk of developing pneumonia, airway infections, headache, and heart failure. It also showed a strong positive correlation with chronic fatigue, a frequently observed symptom in long COVID patients. However, our findings on Parkinson's disease, depression, and chest pain were inconclusive.
CONCLUSION
Overall, these findings provide valuable insights into the genetic underpinnings of long COVID and its diverse range of symptoms. Understanding these causal associations may aid in better management and treatment of long COVID patients, thereby alleviating the substantial burden it poses on global health and socioeconomic systems.
Topics: Humans; Post-Acute COVID-19 Syndrome; COVID-19; Fatigue Syndrome, Chronic; Genome-Wide Association Study; Mendelian Randomization Analysis; Parkinson Disease; SARS-CoV-2; Heart Failure; Chest Pain; Genetic Predisposition to Disease; Headache
PubMed: 38155884
DOI: 10.3389/fpubh.2023.1303183 -
Respiratory Research Nov 2023Chronic obstructive pulmonary disease (COPD), a chronic inflammatory lung disease, is a leading cause of morbidity and mortality worldwide. Prolonged cigarette smoking...
BACKGROUND
Chronic obstructive pulmonary disease (COPD), a chronic inflammatory lung disease, is a leading cause of morbidity and mortality worldwide. Prolonged cigarette smoking (CS) that causes irreversible airway remodeling and significantly reduces lung function is a major risk factor for COPD. Keratin15 (Krt15) cells with the potential of self-renewal and differentiation properties have been implicated in the maintenance, proliferation, and differentiation of airway basal cells; however, the role of Krt15 in COPD is not clear.
METHODS
Krt15 knockout (Krt15) and wild-type (WT) mice of C57BL/6 background were exposed to CS for six months to establish COPD models. Krt15-CrePGR;Rosa26-LSL-tdTomato mice were used to trace the fate of the Krt15 cells. Hematoxylin and eosin (H&E) and Masson stainings were performed to assess histopathology and fibrosis, respectively. Furthermore, lentivirus-delivered short hairpin RNA (shRNA) was used to knock down KRT15 in human bronchial epithelial (HBE) cells stimulated with cigarette smoke extract (CSE). The protein expression was assessed using western blot, immunohistochemistry, and enzyme-linked immunosorbent assay.
RESULTS
Krt15 CS mice developed severe inflammatory cell infiltration, airway remodeling, and emphysema. Moreover, Krt15 knockout aggravated CS-induced secretion of matrix metalloproteinase-9 (MMP-9) and epithelial-mesenchymal transformation (EMT), which was reversed by SB-3CT, an MMP-9 inhibitor. Consistent with this finding, KRT15 knockdown promoted MMP-9 expression and EMT progression in vitro. Furthermore, Krt15 cells gradually increased in the bronchial epithelial cells and were transformed into alveolar type II (AT2) cells.
CONCLUSION
Krt15 regulates the EMT process by promoting MMP-9 expression and protects the lung tissue from CS-induced injury, inflammatory infiltration, and apoptosis. Furthermore, Krt15 cells transformed into AT2 cells to protect alveoli. These results suggest Krt15 as a potential therapeutic target for COPD.
Topics: Animals; Humans; Mice; Airway Remodeling; Cigarette Smoking; Epithelial Cells; Epithelial-Mesenchymal Transition; Keratin-15; Matrix Metalloproteinase 9; Mice, Inbred C57BL; Pulmonary Disease, Chronic Obstructive; Nicotiana
PubMed: 38007424
DOI: 10.1186/s12931-023-02598-w -
The Journal of Biological Chemistry Aug 2023Human neutrophil elastase (HNE) plays a pivotal role in innate immunity, inflammation, and tissue remodeling. Aberrant proteolytic activity of HNE contributes to organ...
Human neutrophil elastase (HNE) plays a pivotal role in innate immunity, inflammation, and tissue remodeling. Aberrant proteolytic activity of HNE contributes to organ destruction in various chronic inflammatory diseases including emphysema, asthma, and cystic fibrosis. Therefore, elastase inhibitors could alleviate the progression of these disorders. Here, we used the systematic evolution of ligands by exponential enrichment to develop ssDNA aptamers that specifically target HNE. We determined the specificity of the designed inhibitors and their inhibitory efficacy against HNE using biochemical and in vitro methods, including an assay of neutrophil activity. Our aptamers inhibit the elastinolytic activity of HNE with nanomolar potency and are highly specific for HNE and do not target other tested human proteases. As such, this study provides lead compounds suitable for the evaluation of their tissue-protective potential in animal models.
Topics: Humans; Cystic Fibrosis; Emphysema; Leukocyte Elastase; Neutrophils; Serine Proteinase Inhibitors; Aptamers, Nucleotide; Sensitivity and Specificity; Enzyme Activation; Proteolysis; Cells, Cultured
PubMed: 37286041
DOI: 10.1016/j.jbc.2023.104889 -
Biomedicine & Pharmacotherapy =... Sep 2023Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity worldwide. Cigarette smoking, which leads to abnormalities in the airways or alveoli and...
Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity worldwide. Cigarette smoking, which leads to abnormalities in the airways or alveoli and persistent obstruction of the airway's flow, is a significant risk factor of COPD. Cryptotanshinone (CTS) is the active ingredient in Salvia miltiorrhiza (Danshen) and has many pharmacological properties including anti-inflammatory, antitumor, and antioxidant properties, but its impact on COPD is uncertain. In the present study, the potential effect of CTS on COPD was investigated in a modified COPD mice model induced with cigarette smoke (CS) and lipopolysaccharide (LPS) exposure. CTS significantly reversed the decline in lung function, emphysema, inflammatory cell infiltration, small airway remodeling, pulmonary pathological damage, and airway epithelial cell proliferation in CS- and LPS-exposed mice. Additionally, CTS decreased inflammatory cytokines such as tumor necrosis factor α (TNF α), interleukins IL-6 and IL-1β, and keratinocyte chemoattractant (KC), increased the activities of superoxide dismutase (SOD), Catalase (CAT) and L-Glutathione (GSH), and repressed the expression of protein hydrolases matrix metalloprotein (MMP)- 9 and - 12 in pulmonary tissue and bronchoalveolar lavage fluid (BALF). The protective effects of CTS were also observed in human bronchial epithelial cell line BEAS-2B simulated with cigarette smoke condensate (CSC) and LPS. Mechanistically, CTS can repress the protein level of Keap1, resulting to activation of erythroid 2-related factor (Nrf2), finally alleviating COPD. In summary, the present findings demonstrated that CTS dramatically ameliorates COPD induced by CS and LPS via activating Keap1/Nrf2 pathway.
Topics: Mice; Humans; Animals; Lipopolysaccharides; NF-E2-Related Factor 2; Cigarette Smoking; Kelch-Like ECH-Associated Protein 1; Pulmonary Disease, Chronic Obstructive; Lung; Nicotiana; Glutathione
PubMed: 37399718
DOI: 10.1016/j.biopha.2023.115105 -
Frontiers in Medicine 2024Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease. Historically, two COPD phenotypes have been described: chronic bronchitis and emphysema.... (Review)
Review
Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease. Historically, two COPD phenotypes have been described: chronic bronchitis and emphysema. Although these phenotypes may provide additional characterization of the pathophysiology of the disease, they are not extensive enough to reflect the heterogeneity of COPD and do not provide granular categorization that indicates specific treatment, perhaps with the exception of adding inhaled glucocorticoids (ICS) in patients with chronic bronchitis. In this review, we describe COPD phenotypes that provide prognostication and/or indicate specific treatment. We also describe COPD-like phenotypes that do not necessarily meet the current diagnostic criteria for COPD but provide additional prognostication and may be the targets for future clinical trials.
PubMed: 38654838
DOI: 10.3389/fmed.2024.1375457 -
Medical Science Monitor : International... Oct 2023The 2023 Global Initiative for Chronic Obstructive Lung Disease (GOLD) report includes relevant topics from the clinician's perspective and evidence published on chronic...
The 2023 Global Initiative for Chronic Obstructive Lung Disease (GOLD) report includes relevant topics from the clinician's perspective and evidence published on chronic obstructive pulmonary disease (COPD) since GOLD 2017. The World Health Organization (WHO) and GOLD 2023 have developed an updated definition of COPD as, "a heterogeneous lung condition characterized by chronic respiratory symptoms (dyspnea, cough, expectoration, exacerbations) due to abnormalities of the airway (bronchitis, bronchiolitis) and/or alveoli (emphysema) that cause persistent, often progressive, airflow obstruction." GOLD 2023 includes recommendations for COPD patients diagnosed with COVID-19 and acknowledges the role of reduced air quality in the etiology and progression of COPD. In May 2023, the GOLD Scientific Committee on Air Pollution and COPD reported that air pollution increasingly contributes to the pathogenesis of COPD. This Editorial aims to introduce the updated GOLD 2023 report in the context of climate change and the aftermath of the COVID-19 pandemic.
Topics: Humans; Climate Change; Pandemics; COVID-19; Pulmonary Disease, Chronic Obstructive; Air Pollution
PubMed: 37777859
DOI: 10.12659/MSM.942672 -
Journal of Thoracic Disease Jun 2023Lung transplantation median survival has seen improvements due to recognition of short-term survival factors but continues to trail behind other solid organs due to...
BACKGROUND
Lung transplantation median survival has seen improvements due to recognition of short-term survival factors but continues to trail behind other solid organs due to limited understanding of long-term survivorship. Given the creation of the United Network for Organ Sharing (UNOS) database in 1986, it was difficult to accrue data on long-term survivors until recently. This study characterizes factors impacting lung transplant survival beyond 20 years, conditional to 1-year survival.
METHODS
Lung transplant recipients listed in UNOS from 1987 to 2002 who survived to 1 post-transplant year were reviewed. Kaplan-Meier and adjusted Cox regression analyses were performed at 20 and 10 years to identify risk factors associated with long-term outcomes independent of their short-term effects.
RESULTS
A total of 6,172 recipients were analyzed, including 472 (7.6%) recipients who lived 20+ years. Factors associated with increased likelihood of 20-year survival were female-to-female gender match, recipient age 25-44, waitlist time >1 year, human leukocyte antigen (HLA) mismatch level 3, and donor cause of death: head trauma. Factors associated with decreased 20-year survival included recipient age ≥55, chronic obstructive pulmonary disease/emphysema (COPD/E) diagnosis, donor smoking history >20 pack-years, unilateral transplant, blood groups O&AB, recipient glomerular filtration rate (GFR) <10 mL/min, and donor GFR 20-29 mL/min.
CONCLUSIONS
This is the first study identifying factors associated with multiple-decade survival following lung transplant in the United States. Despite its challenges, long-term survival is possible and more likely in younger females in good waitlist condition without COPD/E who receive a bilateral allograft from a non-smoking, gender-matched donor of minimal HLA mismatch. Further analysis of the molecular and immunologic implications of these conditions are warranted.
PubMed: 37426158
DOI: 10.21037/jtd-22-1414 -
European Journal of Cardio-thoracic... Oct 2023Screening for lung cancer with low radiation dose computed tomography has a strong evidence base, is being introduced in several European countries and is recommended as... (Review)
Review
BACKGROUND
Screening for lung cancer with low radiation dose computed tomography has a strong evidence base, is being introduced in several European countries and is recommended as a new targeted cancer screening programme. The imperative now is to ensure that implementation follows an evidence-based process that will ensure clinical and cost effectiveness. This European Respiratory Society (ERS) task force was formed to provide an expert consensus for the management of incidental findings which can be adapted and followed during implementation.
METHODS
A multi-European society collaborative group was convened. 23 topics were identified, primarily from an ERS statement on lung cancer screening, and a systematic review of the literature was conducted according to ERS standards. Initial review of abstracts was completed and full text was provided to members of the group for each topic. Sections were edited and the final document approved by all members and the ERS Science Council.
RESULTS
Nine topics considered most important and frequent were reviewed as standalone topics (interstitial lung abnormalities, emphysema, bronchiectasis, consolidation, coronary calcification, aortic valve disease, mediastinal mass, mediastinal lymph nodes and thyroid abnormalities). Other topics considered of lower importance or infrequent were grouped into generic categories, suitable for general statements.
CONCLUSIONS
This European collaborative group has produced an incidental findings statement that can be followed during lung cancer screening. It will ensure that an evidence-based approach is used for reporting and managing incidental findings, which will mean that harms are minimised and any programme is as cost-effective as possible.
Topics: Humans; Lung Neoplasms; Early Detection of Cancer; Expressed Sequence Tags; Incidental Findings; Tomography, X-Ray Computed
PubMed: 37804174
DOI: 10.1093/ejcts/ezad302 -
Journal of Thoracic Disease Nov 2023Tobacco smoking may cause pulmonary perfusion abnormality. Assessment of the lung perfusion characteristics is very significant to timely treatment and prevent disease...
BACKGROUND
Tobacco smoking may cause pulmonary perfusion abnormality. Assessment of the lung perfusion characteristics is very significant to timely treatment and prevent disease progression in smokers. The purpose was to investigate the value of iodine maps from spectral dual-layer detector computed tomography (DLCT) in assessing lung perfusion changes in smokers.
METHODS
Nineteen smokers and 29 non-smokers who underwent dual-phase contrast enhanced scans on a spectral DLCT were retrospectively collected. Emphysema on non-contrast images and perfusion defect (PD) on iodine maps were scored visually at bilateral lung fields of three anatomic levels (on the slice of the aortic arch, the carina, and the aperture of the inferior pulmonary veins). The scores were calculated based on the ratio of the abnormality occupied in the pulmonary field of each slice as described below: point 0, no abnormality; point 1, 0%< abnormality scope ≤25%; points 2, 25%< abnormality scope ≤50%; points 3, 50%< abnormality scope ≤75%; points 4, abnormality scope >75%. The sum of scores for each patient was calculated. The iodine density (ID) of PD and thoracic aorta were measured respectively (ID, ID), then calculating the ratio as the normalized ID (nID). Emphysema index (EI) was defined as the volume percentage of the lung attenuation below -950 Hounsfield units. The percentage of forced expiratory volume in 1 second (FEV) to the predicted value (FEV%) and the ratio of FEV to forced vital capacity (FVC) were recorded. The differences of the emphysema and PD visual scores, ID, nID, EI were analyzed by analysis of variance between smokers and non-smokers. Correlations between emphysema, PD and FEV%, FEV/FVC were evaluated by Spearman correlation analysis.
RESULTS
The PD visual scores on ID images were significantly higher in smokers compared with that in non-smokers (P=0.014), while no significantly difference was found for emphysema visual scores (P=0.402). Both ID and nID were significantly lower in smokers compared with non-smokers (P=0.003; P=0.029), while no significantly difference was found for EI (P=0.061). Besides, PD visual scores were negatively correlated with FEV% (r=-0.61, P=0.025) and FEV/FVC (r=-0.62, P=0.024) for smokers.
CONCLUSIONS
Compared with emphysema, the iodine map derived from spectral DLCT showed higher sensitivity for the evaluation of the pulmonary abnormalities of smokers.
PubMed: 38090318
DOI: 10.21037/jtd-23-891