Small airway remodeling in diabetic and smoking chronic obstructive pulmonary disease patients

Wu, Nan; Wu, Zhenchao; Sun, Jian; Yan, Mengdie; Wang, Bingbing; Du, Xu; Liu, Yi

doi:10.18632/aging.103112

Cited by 12 publications

(12 citation statements)

References 37 publications

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“…In addition, TGF-β1 expression was significantly increased in the airway epithelium of both smokers and COPD patients, accompanied by the expression of ρ Smad2/3 [16,106]. Likewise, cigarette smoke induces EMT in lung and bronchial epithelial cells through TGF-β1/ Smad signaling pathway in vivo and in vitro [107][108][109][110][111]. Together, these studies suggest that cigarette smoke targeting the TGF-β/Smad signaling pathway induces EMT in COPD.…”

Section: Tgf-β/smad Signaling Pathwaymentioning

confidence: 75%

The effects of epithelial–mesenchymal transitions in COPD induced by cigarette smoke: an update

Zhu

Lin

et al. 2022

Respir Res

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Cigarette smoke is a complex aerosol containing a large number of compounds with a variety of toxicity and carcinogenicity. Long-term exposure to cigarette smoke significantly increases the risk of a variety of diseases, including chronic obstructive pulmonary disease (COPD) and lung cancer. Epithelial–mesenchymal transition (EMT) is a unique biological process, that refers to epithelial cells losing their polarity and transforming into mobile mesenchymal cells, playing a crucial role in organ development, fibrosis, and cancer progression. Numerous recent studies have shown that EMT is an important pathophysiological process involved in airway fibrosis, airway remodeling, and malignant transformation of COPD. In this review, we summarized the effects of cigarette smoke on the development and progression of COPD and focus on the specific changes and underlying mechanisms of EMT in COPD induced by cigarette smoke. We spotlighted the signaling pathways involved in EMT induced by cigarette smoke and summarize the current research and treatment approaches for EMT in COPD, aiming to provide ideas for potential new treatment and research directions.

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Section: Tgf-β/smad Signaling Pathwaymentioning

confidence: 75%

The effects of epithelial–mesenchymal transitions in COPD induced by cigarette smoke: an update

Zhu

Lin

et al. 2022

Respir Res

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“…In a study by Postma Dirkje S, SAD was found to be a risk factor for asthma and was present at all levels of asthma [ 47 ], particularly in patients with severe asthma. However, another study identified asthma as a risk factor for small airway disorders [ 48 ]. One study contradicted the idea that inhaling allergic or nonallergic irritants causes inflammation or contraction of smooth muscles, which reduces their diameter and increases airway resistance, leading to SAD.…”

Section: Discussionmentioning

confidence: 99%

Analysis of influencing factors and a predictive model of small airway dysfunction in adults

Zhang

et al. 2023

BMC Pulm Med

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Background Small airway dysfunction (SAD) is a widespread but less typical clinical manifestation of respiratory dysfunction. In lung diseases, SAD can have a higher-than-expected impact on lung function. The aim of this study was to explore risk factors for SAD and to establish a predictive model. Methods We included 1233 patients in the pulmonary function room of TangDu Hospital from June 2021 to December 2021. We divided the subjects into a small airway disorder group and a non-small airway disorder group, and all participants completed a questionnaire. We performed univariate and multivariate analyses to identify the risk factors for SAD. Multivariate logistic regression was performed to construct the nomogram. The performance of the nomogram was assessed and validated by the Area under roc curve (AUC), calibration curves, and Decision curve analysis (DCA). Results One. The risk factors for small airway disorder were advanced age (OR = 7.772,95% CI 2.284–26.443), female sex (OR = 1.545,95% CI 1.103–2.164), family history of respiratory disease (OR = 1.508,95% CI 1.069–2.126), history of occupational dust exposure (OR = 1.723,95% CI 1.177–2.521), history of smoking (OR = 1.732,95% CI 1.231–2.436), history of pet exposure (OR = 1.499,95% CI 1.065–2.110), exposure to O3 (OR = 1.008,95% CI 1.003–1.013), chronic bronchitis (OR = 1.947,95% CI 1.376–2.753), emphysema (OR = 2.190,95% CI 1.355–3.539) and asthma (OR = 7.287,95% CI 3.546–14.973). 2. The AUCs of the nomogram were 0.691 in the training set and 0.716 in the validation set. Both nomograms demonstrated favourable clinical consistency. 3.There was a dose‒response relationship between cigarette smoking and SAD; however, quitting smoking did not reduce the risk of SAD. Conclusion Small airway disorders are associated with age, sex, family history of respiratory disease, occupational dust exposure, smoking history, history of pet exposure, exposure to O3, chronic bronchitis, emphysema, and asthma. The nomogram based on the above results can effectively used in the preliminary risk prediction.

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“…3,27,37 Furthermore, high glucose exposure induces epithelial-mesenchymal transition (EMT) via the transforming growth factor beta (TGF-β)/Smad pathway in airway epithelial cells (AECs), which induces small airway dysfunction. 13 Whether diabetes control can lower COPD risk needs to be confirmed in future clinical trials.…”

Section: Discussionmentioning

confidence: 99%

“…7,11,12 A recent observational study also found that the small airway dysfunction and airflow limitations were worse in COPD patients with a history of diabetes. 13 Furthermore, several prospective studies have shown that COPD patients with diabetes are at a higher risk of severe exacerbation and death. 4,5,14 In addition, a cohort study based on the United Kingdom Clinical Practice Research Datalink reported that the use of antidiabetic drugs was associated with a reduced risk of severe exacerbations in COPD patients.…”

Section: Introductionmentioning

confidence: 99%

Associations of diabetes, prediabetes and diabetes duration with the risk of chronic obstructive pulmonary disease: A prospective UK Biobank study

Wan

et al. 2023

Diabetes Obesity Metabolism

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Aim: To investigate the associations of diabetes, prediabetes and diabetes duration with chronic obstructive pulmonary disease (COPD) risk and survival in the UK Biobank. Materials and Methods:We conducted a prospective analysis among 452 680 participants without COPD at baseline using UK Biobank data. Multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated from Cox regression models. The dose-response relationship was explored using restricted cubic splines. A separate survival analysis was conducted for 12 595 patients with incident COPD.Results: Over a median follow-up of 12.3 years, 12 595 cases of COPD were documented. Compared with the reference group, those with prediabetes and diabetes were associated with an 18% (HR 1.18 [95% CI: 1.13-1.24]) and 35% (HR 1.35 [95% CI: 1.24-1.47]) higher risk of COPD, respectively. Diabetes duration was associated with COPD risk, with multivariable HRs (95% CIs) of 1.23 (1.05-1.44), 1.20 (1.04-1.39) and 1.18 (1.01-1.37) for diabetes duration of 7 years or longer, 3 to less than 7 years, and 1 to less than 3 years versus less than 1 year, respectively. Doseresponse analysis revealed a non-linear relationship between diabetes duration and COPD risk. Regarding COPD survival, COPD patients with prediabetes and diabetes had a 9% (HR 1.09 [95% CI: 1.00-1.19]) and 21% (HR 1.21 [95% CI: 1.05-1.41]) higher risk of overall death, respectively. Compared with the cases with a diabetes duration of less than 1 year, those with a diabetes duration of 7 years or longer were associated with a 46% higher risk of overall death ).

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Small airway remodeling in diabetic and smoking chronic obstructive pulmonary disease patients

Abstract: Numerous diseases have been found to coexist with COPD, including cardiovascular disease, osteoporosis, lung cancer and so on [3-5]. A clinical trial demonstrated www.aging-us.com

Cited by 12 publications

References 37 publications

The effects of epithelial–mesenchymal transitions in COPD induced by cigarette smoke: an update

The effects of epithelial–mesenchymal transitions in COPD induced by cigarette smoke: an update

Analysis of influencing factors and a predictive model of small airway dysfunction in adults

Associations of diabetes, prediabetes and diabetes duration with the risk of chronic obstructive pulmonary disease: A prospective UK Biobank study

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