The Role of Smoking in the Mechanisms of Development of Chronic Obstructive Pulmonary Disease and Atherosclerosis

Kotlyarov, Stanislav

doi:10.3390/ijms24108725

Cited by 21 publications

(6 citation statements)

References 247 publications

(273 reference statements)

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“…In the heart and vasculature, ROS inflict oxidative damage on LDL particles, while inflammation accelerates atherosclerotic plaque formation. In reproductive tissues, carcinogens in cigarette smoke penetrate cervical mucus and are absorbed systemically, contributing to cancers of the lung, cervix, bladder and pancreas (Kotlyarov 2023).…”

Section: Mechanisms Of Smoking-induced Diseasementioning

confidence: 99%

Oxidative stress and inflammation: elucidating mechanisms of smoking-attributable pathology for therapeutic targeting

Addissouky,

El Sayed,

Ali

et al. 2024

Bull Natl Res Cent

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Background Tobacco smoking remains a major preventable cause of disease and death worldwide. Combustible cigarettes release thousands of chemicals that can initiate inflammatory pathways leading to smoking-related illness. This review aims to synthesize current scientific knowledge on mechanisms of smoking-induced disease, epidemiological trends, and clinical strategies from recent literature. Main body of the abstract At the cellular level, cigarette smoke triggers oxidative stress through reactive oxygen species (ROS), causing DNA damage. This provokes inflammatory signaling cascades mediated by damage-associated molecular patterns (DAMPs), receptors like RAGE and TLRs, and downstream cytokines. Smoking also disrupts apoptosis and autophagy. In the lungs, oxidative stress and inflammation from smoking play central roles in COPD pathogenesis. Smoking-induced oxidative DNA damage, chronic inflammation, and impaired immunity combine to promote lung carcinogenesis. For cardiovascular disease, smoking triggers endothelial dysfunction, platelet activation, and atherogenesis through oxidized LDL and effects on nitric oxide and adhesion molecules. Short conclusion Given the unequivocal evidence of health risks, smoking cessation is critical to reducing preventable death and disability. Both counseling and pharmacotherapy have proven efficacy for quitting, but efficacy remains limited long-term. Emerging nicotine products like e-cigarettes have unknown impacts on cessation and population health. Comprehensive efforts encompassing prevention, screening, treatment innovation, harm reduction, and policy reform focused on curbing smoking-attributable morbidity and mortality are warranted.

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Section: Mechanisms Of Smoking-induced Diseasementioning

confidence: 99%

Oxidative stress and inflammation: elucidating mechanisms of smoking-attributable pathology for therapeutic targeting

Addissouky,

El Sayed,

Ali

et al. 2024

Bull Natl Res Cent

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“…In addition, the OS group comprised expectedly of a greater proportion of patients with smoking history and had higher BMI values than the OSA group. It is well known the effects of smoking [43] and obesity [44,45] increase the risk of CVD independently of the presence of COPD and OSA, respectively. However, after controlling for confounding factors, neither smoking history nor BMI independently correlated with hs-TnT and NT-proBNP serum levels in the present study.…”

Section: Limitationsmentioning

confidence: 99%

Is COPD the Determinant Factor for Myocardial Injury and Cardiac Wall Stress in OSA Patients?

Voulgaris,

Archontogeorgis,

Apessos

et al. 2023

Medicina

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Background and Objectives: Evidence shows that COPD-OSA overlap syndrome (OS) is more frequently accompanied by cardiovascular disease (CVD) in comparison to either disease alone. The aim of the study was to explore whether patients with OS have a higher burden of subclinical myocardial injury and wall stress compared with OSA patients. Materials and Methods: Consecutive patients, without established CVD, underwent polysomnography and pulmonary function testing, due to suspected sleep-disordered breathing. An equal number of patients with OS (n = 53, with an apnea hypopnea index (AHI) > 5/h and FEV1/FVC < 0.7) and patients with OSA (n = 53, AHI > 5/h and FEV1/FVC > 0.7) were included in the study. The detection of asymptomatic myocardial injury and wall stress was performed via the assessment of serum high-sensitivity cardiac troponin T (hs-cTnT) and N-terminal pro-B-type natriuretic peptide (NT-proBNP), respectively. Results: OS patients were older (p < 0.001) and had worse hypoxemic parameters, namely average oxyhemoglobin saturation (SpO2) (p = 0.002) and time spent with SpO2 < 90% (p = 0.003) during sleep as well as daytime pO2 (p < 0.001), than patients with OSA. No difference was observed between groups in terms of Epworth Sleepiness Scale (p = 0.432) and AHI (p = 0.587). Both levels of hs-cTnT (14.2 (9.1–20.2) vs. 6.5 (5.6–8.7) pg/mL, p < 0.001) and NT-proBNP (93.1 (37.9–182.5) vs. 19.2 (8.3–35.4) pg/mL, p < 0.001) were increased in OS compared to OSA patients. Upon multivariate linear regression analysis, levels of NT-proBNP and hs-cTnT correlated with age and average SpO2 during sleep. Conclusions: Our study demonstrated higher levels of hs-cTnT and NT-proBNP in OS patients, indicating an increased probability of subclinical myocardial injury and wall stress, compared with OSA individuals.

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“…The upregulation of inflammatory pathways increases pro-inflammatory cytokines such as TNF-α, IL-6, IL-8, and IL-1β, which play crucial roles in COPD pathophysiology [ 6 ]. Therefore, inflammatory markers are elevated in COPD and can be quantified to detect severity, prognosis, mortality risk, and response to treatment, albeit with high cost.…”

Section: Introductionmentioning

confidence: 99%

Neutrophil-to-Lymphocyte Ratio and Blood Eosinophil Levels As Inflammatory Indicators in Smoker and Non-smoker Young Adult Patients With Chronic Obstructive Pulmonary Disease at a Tertiary Care Hospital

Waseem,

Masood,

Siddiqui

et al. 2024

Cureus

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Background Inflammatory markers are elevated in chronic obstructive pulmonary disease (COPD) and can be quantified to detect severity, prognosis, mortality risk, and response to treatment. However, the estimation costs are high. The blood neutrophil-to-lymphocyte ratio (NLR) and eosinophil levels are emerging as biomarkers in COPD, yet there is a paucity of data. Aim and objectives This study was designed to elucidate the roles of the NLR and eosinophil levels in smokers and non-smokers with stable COPD male subjects, correlating them with lung functions. Materials and methods A prospective observational clinical study was conducted from January to June 2023, after receiving approval from the Institutional Ethics Committee, on 73 COPD patients aged 30-60 years who gave voluntary informed consent. Complete blood counts and spirometry were performed. Patients with a forced expiratory volume in one second (FEV1) % predicted <70% and an FEV1/forced vital capacity (FVC) % <70% based on the pulmonary function test (MIR Spirolab) were included. They were further divided into mild (n=10), moderate (n=27), severe (n=26), and very severe (n=10) categories as per the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines. Subjects were also categorized into smoker (n=45) and non-smoker (n=28) groups. The complete blood count was analyzed using an automated analyzer (Beckman Coulter). Analysis was also carried out with an NLR of more or less than three. A P-value of less than 0.05 was considered significant. Results Smokers constituted 61.65% (n=45) of the subjects, and non-smokers 38.35% (n=28). Among smokers, 17.78% had very severe airflow obstruction. In all COPD subjects (n=73), lymphocytes, eosinophils, and lung functions were lower in the group where the NLR was greater than three. NLR in smokers (3.52±1.43) was higher than in non-smokers (3.39±0.94). In non-smokers (n=28), blood eosinophils and lymphocytes were elevated. In smokers (n=45), blood neutrophils, monocytes, and basophils were increased. Smokers showed a non-significant increase in RBC, mean corpuscular volume (MCV), and mean corpuscular hemoglobin (MCH). Neutrophils, monocytes, eosinophils, and NLR increased with disease severity. NLR negatively correlated with FEV1 (r=-0.350, p=0.034) and positively with pack-years (r=0.546, p<0.001) in smokers. NLR negatively correlated with eosinophils, FVC, FEV1/FVC, and FEV1 % predicted. In all COPD subjects (n=73), NLR negatively correlated with blood eosinophils (r=-0.184, p=0.12), BMI, and lung functions. Conclusion NLR is elevated in COPD subjects and can serve as a marker of inflammation and a predictor of the risk and severity of airflow limitation. NLR correlates both positively and negatively with pack-years and lung functions, respectively.

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The Role of Smoking in the Mechanisms of Development of Chronic Obstructive Pulmonary Disease and Atherosclerosis

Cited by 21 publications

References 247 publications

Oxidative stress and inflammation: elucidating mechanisms of smoking-attributable pathology for therapeutic targeting

Oxidative stress and inflammation: elucidating mechanisms of smoking-attributable pathology for therapeutic targeting

Is COPD the Determinant Factor for Myocardial Injury and Cardiac Wall Stress in OSA Patients?

Neutrophil-to-Lymphocyte Ratio and Blood Eosinophil Levels As Inflammatory Indicators in Smoker and Non-smoker Young Adult Patients With Chronic Obstructive Pulmonary Disease at a Tertiary Care Hospital

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