scholarly journals COPD and stroke: are systemic inflammation and oxidative stress the missing links?

2016 ◽  
Vol 130 (13) ◽  
pp. 1039-1050 ◽  
Author(s):  
Victoria Austin ◽  
Peter J. Crack ◽  
Steven Bozinovski ◽  
Alyson A. Miller ◽  
Ross Vlahos
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Systemic Inflammation ◽  
Vascular Dysfunction ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Cardiovascular Comorbidities ◽  
Shared Risk ◽  
And Oxidative Stress

Chronic obstructive pulmonary disease (COPD) is characterized by progressive airflow limitation and loss of lung function, and is currently the third largest cause of death in the world. It is now well established that cardiovascular-related comorbidities such as stroke contribute to morbidity and mortality in COPD. The mechanisms linking COPD and stroke remain to be fully defined but are likely to be interconnected. The association between COPD and stroke may be largely dependent on shared risk factors such as aging and smoking, or the association of COPD with traditional stroke risk factors. In addition, we propose that COPD-related systemic inflammation and oxidative stress may play important roles by promoting cerebral vascular dysfunction and platelet hyperactivity. In this review, we briefly discuss the pathogenesis of COPD, acute exacerbations of COPD (AECOPD) and cardiovascular comorbidities associated with COPD, in particular stroke. We also highlight and discuss the potential mechanisms underpinning the link between COPD and stroke, with a particular focus on the roles of systemic inflammation and oxidative stress.

scholarly journals New frontiers in the treatment of comorbid cardiovascular disease in chronic obstructive pulmonary disease

2019 ◽  
Vol 133 (7) ◽  
pp. 885-904 ◽  
Author(s):  
Kurt Brassington ◽  
Stavros Selemidis ◽  
Steven Bozinovski ◽  
Ross Vlahos
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Chronic Obstructive Pulmonary Disease ◽  
Blood Vessel ◽  
Pulmonary Disease ◽  
Vascular Endothelial Cells ◽  
Vascular Dysfunction ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

Abstract Chronic obstructive pulmonary disease (COPD) is a disease characterised by persistent airflow limitation that is not fully reversible and is currently the fourth leading cause of death globally. It is now well established that cardiovascular-related comorbidities contribute to morbidity and mortality in COPD, with approximately 50% of deaths in COPD patients attributed to a cardiovascular event (e.g. myocardial infarction). Cardiovascular disease (CVD) and COPD share various risk factors including hypertension, sedentarism, smoking and poor diet but the underlying mechanisms have not been fully established. However, there is emerging and compelling experimental and clinical evidence to show that increased oxidative stress causes pulmonary inflammation and that the spill over of pro-inflammatory mediators from the lungs into the systemic circulation drives a persistent systemic inflammatory response that alters blood vessel structure, through vascular remodelling and arterial stiffness resulting in atherosclerosis. In addition, regulation of endothelial-derived vasoactive substances (e.g. nitric oxide (NO)), which control blood vessel tone are altered by oxidative damage of vascular endothelial cells, thus promoting vascular dysfunction, a key driver of CVD. In this review, the detrimental role of oxidative stress in COPD and comorbid CVD are discussed and we propose that targeting oxidant-dependent mechanisms represents a novel strategy in the treatment of COPD-associated CVD.

scholarly journals Cardiovascular diseases and chronic obstructive pulmonary disease: etiopathogenetic relationship and clinical signifi cance (literature review)

2020 ◽  
Vol 35 (2) ◽  
pp. 26-34
Author(s):  
A. M. Chaulin ◽  
D. V. Duplyakov
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Chronic Obstructive Pulmonary Disease ◽  
Cardiovascular Diseases ◽  
Pulmonary Disease ◽  
Sedentary Lifestyle ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
The Relationship ◽  
And Oxidative Stress

Cardiovascular diseases (CVD) and chronic obstructive pulmonary disease (COPD) often coexist. Comorbidity of CVD and COPD is a serious modern medical and social problem. This article discusses the main risk factors that are common for COPD and CVD: smoking, infl ammation, a sedentary lifestyle, aging, and oxidative stress. Pathogenetic mechanisms underlying the relationship between COPD and CVD are also discussed.

scholarly journals A literature review on depression and its risk factors among people suffering from chronic obstructive pulmonary disease in Asian sub-continent

2020 ◽  
Vol 7 (11) ◽  
pp. 4653
Author(s):  
Amrit Sharma
Keyword(s):  
Risk Factors ◽  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Low Income ◽  
Airflow Obstruction ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Chronic Inflammatory Response ◽  
Basic Activity

Chronic obstructive pulmonary disease (COPD) is defined as persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. It has been suggested that emotional disturbances such as depression and anxiety are common among patients with COPD. This review aims to highlight the presence of depression and associated risk factors among patients suffering from COPD in Asia. Fifty-eight observational studies were retrieved through data sources like PubMed, Medical subject heading (MeSH) search and Google scholar. After thorough screening total thirteen studies were identified and included in this review. Based on the results of these studies, the south and west Asian countries had higher proportion of depression. However, risk factor results were mixed which includes severity of obstruction/global initiative for obstructive lung disease (GOLD) criteria, Stage 2 COPD, teetotallers, smoking, alcohol consumption, body mass index, airflow obstruction, dyspnoea, and exercise (BODE) index, urban residence, female gender, education level, dyspnoea, low income, poor Quality of life (QOL) scores, age, poor self-reported health, basic activity of daily living (BADL) disability. Further superior research studies with larger sample size are required on Asian population. All in all, it is recommended that early diagnosis and treatment of depression should be included as a part of management in COPD as it can help to minimize the risk of morbidity and mortality in the patients.

scholarly journals Cardiovascular Comorbidities in Chronic Obstructive Pulmonary Disease (COPD)—Current Considerations for Clinical Practice

2019 ◽  
Vol 8 (1) ◽  
pp. 69 ◽  
Author(s):  
Frederik Trinkmann ◽  
Joachim Saur ◽  
Martin Borggrefe ◽  
Ibrahim Akin
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Cardiovascular Comorbidities ◽  
Disease Entities ◽  
Considerable Morbidity ◽  
The Individual ◽  
Shared Risk ◽  
Current Guidelines

In patients with chronic obstructive pulmonary disease (COPD), cardiovascular comorbidities are highly prevalent and associated with considerable morbidity and mortality. This coincidence is increasingly seen in context of a “cardiopulmonary continuum” rather than being simply attributed to shared risk factors such as cigarette smoking. Overlapping symptoms such as dyspnea or chest pain lead to a worse prognosis due to missed concomitant diagnoses. Moreover, medication is often withheld as a result of unfounded concerns about side effects. Despite the frequent coincidence, current guidelines are still mostly restricted to the management of the individual disease. Future diagnostic and therapeutic strategies should therefore be guided by an integrative perspective as well as a refined phenotyping of disease entities.

scholarly journals Hypogonadism in chronic obstructive pulmonary disease (COPD): Risk factors

2019 ◽  
Vol 76 (1) ◽  
pp. 55-60
Author(s):  
Ljiljana Novkovic ◽  
Zorica Lazic ◽  
Marina Petrovic ◽  
Vojislav Cupurdija ◽  
Katarina Vujanac ◽  
...  
Keyword(s):  
Risk Factors ◽  
Chronic Obstructive Pulmonary Disease ◽  
Skeletal Muscle ◽  
Gas Exchange ◽  
Pulmonary Disease ◽  
Systemic Inflammation ◽  
Independent Predictor ◽  
Free Testosterone ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

Bacground/Aim. Chronic obstructive pulmonary disease (COPD) is the leading cause of morbidity and mortality in pulmonary pathology. However, apart from its own pulmonary manifestations, this disease is also characterized by systemic effects, including hypogonadism which is described especially in the group of men with COPD. The aim of this study was to evaluate risk factors for hypogonadism in men with COPD. Methods. The study included 96 male patients with COPD in stable phase of the disease. All patients were checked for concentration of free testosterone in serum, markers of systemic inflammation, tumor necrosis factor-? (TNF-?), interleukin-1? (IL-1?) and C reactive protein (CRP), pulmonary function test, gas exchange parameters, a 6-minute walk test (6MWT), nutritional status and condition of skeletal muscle (midthigh muscle cross-sectional area ? MTCSA using computed tomography). Results. Decreased value of free testosterone was found in 37.5% of the patients. In the group with hypogonadism (free testosterone < 4.5 pg/mL), we found significantly increased serum concentration of TNF-? (5.88 ? 3.21 vs. 3.16 ? 2.53 pg/mL; p < 0.05), significantly lower MTSCA (68.2 ? 18.72 vs. 91.1 ? 21.4 cm2; p < 0.05) and the 6MWT (268.33 ? 32.35 vs. 334.25 ? 43.25 m; p < 0.05). Lung function, gas exchange markers and body mass index (BMI) were similar in both groups. The multivariate regression analysis singled out serum value of TNF-? as an independent predictor of serum concentrations of free testosterone (B = -0.157; 95% confidence interval: -0.262?0.053). Conclusion. In our analysis we found that TNF-? as a marker of systemic inflammation is an independent predictor of the presence of hypogonadism in the patients with COPD. Our results indicate that hypogonadism predisposes to skeletal muscle wasting and exercise intolerance in male COPD patients.

PI3K/Akt-Nrf2 and Anti-Inflammation Effect of Macrolides in Chronic Obstructive Pulmonary Disease

2019 ◽  
Vol 20 (4) ◽  
pp. 301-304 ◽  
Author(s):  
Xuejiao Sun ◽  
Lin Chen ◽  
Zhiyi He
Keyword(s):  
Oxidative Stress ◽  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Systemic Inflammation ◽  
Inflammatory Responses ◽  
Protective Role ◽  
Akt Pathway ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Inflammatory Mechanism

Background: Chronic Obstructive Pulmonary Disease (COPD) is a systematic inflammatory disease, and smoking is an important risk factor for COPD. Macrolide can reduce COPD inflammation. However, the inflammatory mechanism of COPD remains unclear and the anti-inflammatory mechanism of Macrolide is complex and not exactly known. Methods: We read and analysed thirty-eight articles, including original articles and reviews. Results: The expression of Nrf2 was lower in COPD patients and might have a protective role against apoptosis caused by CSE-induced oxidative stress. Nrf2 may play an important role in COPD inflammation. Nrf2 is a key factor in downstream of PI3K/Akt and is involved in the regulation of oxidative stress and inflammatory response. Therefore, PI3K/Akt pathway may play an important role in the activation of Nrf2 and COPD inflammation. Macrolide reduces lung and systemic inflammation of COPD by regulating PI3K/Akt pathway. Conclusion: This review indicates that PI3K/Ak-Nrf2 may play an important role in COPD inflammation and macrolides may reduce lung and systemic inflammation of COPD by regulating PI3K/Akt-Nrf2 pathway. However, many crucial and essential questions remain to be answered. Further understanding of the mechanisms of macrolide efficacy and PI3K/Akt-Nrf2-mediated inflammatory responses may provide a new clue for exploring COPD treatment in the future.

Smoking, Systemic Inflammation, and Airflow Limitation: A Mendelian Randomization Analysis of 98 085 Individuals From the General Population

2018 ◽  
Vol 21 (8) ◽  
pp. 1036-1044 ◽  
Author(s):  
Yunus Çolak ◽  
Shoaib Afzal ◽  
Peter Lange ◽  
Børge G Nordestgaard
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
General Population ◽  
Pulmonary Disease ◽  
Systemic Inflammation ◽  
Tobacco Consumption ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
General Population Study ◽  
Former Smokers

Abstract Introduction Smoking is associated with systemic and local inflammation in the lungs. Furthermore, in chronic obstructive pulmonary disease, which is often caused by smoking, there is often systemic inflammation that is linked to lung function impairment. However, the causal pathways linking smoking, systemic inflammation, and airflow limitation are still unknown. We tested whether higher tobacco consumption is associated with higher systemic inflammation, observationally and genetically and whether genetically higher systemic inflammation is associated with airflow limitation. Methods We included 98 085 individuals aged 20–100 years from the Copenhagen General Population Study; 36589 were former smokers and 16172 were current smokers. CHRNA3 rs1051730 genotype was used as a proxy for higher tobacco consumption and the IL6R rs2228145 genotype was used for higher systemic inflammation. Airflow limitation was defined as forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC) <70%. Results Difference in plasma level of C-reactive protein was 4.8% (95% CI = 4.4% to 5.2%) per 10 pack-year increase and 1.6% (95% CI = 0.4% to 2.8%) per T allele. Corresponding differences were 1.2% (95% CI = 1.1% to 1.3%) and 0.5% (95% CI = 0.3% to 0.8%) for fibrinogen, 1.2% (95% CI = 1.2% to 1.3%) and 0.7% (95% CI = 0.5% to 1.0%) for α1-antitrypsin, 2.0% (95% CI = 1.8% to 2.1%) and 0.7% (95% CI = 0.4% to 1.1%) for leukocytes, 1.9% (95% CI = 1.8% to 2.1%) and 0.8% (95% CI = 0.4% to 1.2%) for neutrophils, and 0.8% (95% CI = 0.7% to 1.0%) and 0.4% (95% CI = 0.1% to 0.7%) for thrombocytes. The differences in these levels were lower for former smokers compared with current smokers. The IL6R rs2228145 genotype was associated with higher plasma acute-phase reactants but not with airflow limitation. Compared with the C/C genotype, the odds ratio for airflow limitation was 0.95 (95% CI = 0.89 to 1.02) for A/C genotype and 0.94 (95% CI = 0.87 to 1.01) for A/A genotype. Conclusions Higher tobacco consumption is associated with higher systemic inflammation both genetically and observationally, whereas systemic inflammation was not associated with airflow limitation genetically. Implications The association between higher tobacco consumption and higher systemic inflammation may be causal, and the association is stronger among current smokers compared to former smokers, indicating that smoking cessation may reduce the effects of smoking on systemic inflammation. Systemic inflammation does not seem to be a causal driver in development of airflow limitation. These findings can help to understand the pathogenic effects of smoking and the interplay between smoking, systemic inflammation, and airflow limitation and hence development and progression of chronic obstructive pulmonary disease.

scholarly journals Reliability and Usefulness of Different Biomarkers of Oxidative Stress in Chronic Obstructive Pulmonary Disease

2020 ◽  
Vol 2020 ◽  
pp. 1-12 ◽  
Author(s):  
Elisabetta Zinellu ◽  
Angelo Zinellu ◽  
Alessandro G. Fois ◽  
Sara S. Fois ◽  
Barbara Piras ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Analytical Methods ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Oxidative Stress Biomarkers ◽  
Obstructive Pulmonary Disease ◽  
Stress Biomarkers ◽  
Biomarkers Of Oxidative Stress

Introduction. Chronic obstructive pulmonary disease (COPD) is a progressive disease characterized by airflow limitation that is not fully reversible after inhaled bronchodilator use associated with an abnormal inflammatory condition. The biggest risk factor for COPD is cigarette smoking. The exposure to noxious chemicals contained within tobacco smoke is known to cause airway epithelial injury through oxidative stress, which in turn has the ability to elicit an inflammatory response. In fact, the disruption of the delicate balance between oxidant and antioxidant defenses leads to an oxidative burden that has long been held responsible to play a pivotal role in the pathogenesis of COPD. There are currently several biomarkers of oxidative stress in COPD that have been evaluated in a variety of biological samples. The aim of this review is to identify the best studied molecules by summarizing the key literature findings, thus shedding some light on the subject. Methods. We searched for relevant case-control studies examining oxidative stress biomarkers in stable COPD, taking into account the analytical method of detection as an influence factor. Results. Many oxidative stress biomarkers have been evaluated in several biological matrices, mostly in the blood. Some of them consistently differ between the cases and controls even when allowing different analytical methods of detection. Conclusions. The present review provides an overview of the oxidative stress biomarkers that have been evaluated in patients with COPD, bringing focus on those molecules whose reliability has been confirmed by the use of different analytical methods.

scholarly journals Induced sputum metabolomic profiles and oxidative stress are associated with chronic obstructive pulmonary disease (COPD) severity: potential use for predictive, preventive, and personalized medicine

2020 ◽  
Vol 11 (4) ◽  
pp. 645-659
Author(s):  
Tao Zhu ◽  
Shanqun Li ◽  
Jiajia Wang ◽  
Chunfang Liu ◽  
Lei Gao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Obstructive Pulmonary Disease ◽  
Induced Sputum ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Preventive And Personalized Medicine ◽  
And Personalized Medicine ◽  
And Oxidative Stress ◽  
Severe Copd

AbstractChronic obstructive pulmonary disease (COPD) is a highly heterogeneous disease, and metabolomics plays a hub role in predictive, preventive, and personalized medicine (PPPM) related to COPD. This study thus aimed to reveal the role of induced sputum metabolomics in predicting COPD severity. In this pilot study, a total of 20 COPD patients were included. The induced sputum metabolites were assayed using a liquid chromatography-mass spectrometry (LC-MS/MS) system. Five oxidative stress products (myeloperoxidase (MPO), superoxide dismutase (SOD), glutathione (GSH), neutrophil elastase (NE), and 8-iso-PGF2α) in induced sputum were measured by ELISA, and the metabolomic profiles were distinguished by principal component analysis (PCA) and orthogonal projections to latent structures discriminant analysis (OPLS-DA). The Kyoto Encyclopedia of Genes and Genomes (KEGG) was used for pathway enrichment analysis, and a significant difference in induced sputum metabolomics was observed between moderate and severe COPD. The KEGG analysis revealed that the glycerophospholipid metabolism pathway was downregulated in severe COPD. Due to the critical role of glycerophospholipid metabolism in oxidative stress, significant negative correlations were discovered between glycerophospholipid metabolites and three oxidative stress products (SOD, MPO, and 8-iso-PGF2α). The diagnostic values of SOD, MPO, and 8-iso-PGF2α in induced sputum were found to exhibit high sensitivities and specificities in the prediction of COPD severity. Collectively, this study provides the first identification of the association between induced sputum metabolomic profiles and COPD severity, indicating the potential value of metabolomics in PPPM for COPD management. The study also reveals the correlation between glycerophospholipid metabolites and oxidative stress products and their value for predicting COPD severity.

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