Department of Anesthesiology and Reanimation, Faculty of Medicine, Mardin Artuklu University, Mardin 47200, Turkey.
Department of Anesthesiology and Reanimation, Mardin Training and Research Hospital, Mardin 47000, Turkey.
Medicina (Kaunas). 2024 Oct 24;60(11):1750. doi: 10.3390/medicina60111750.
Small airway fibrosis plays a critical role in the progression of chronic obstructive pulmonary disease (COPD). Previous research has suggested that Urotensin-II (U-II) and transforming growth factor-β (TGF-β) may contribute to pathological fibrosis in various organs, including the cardiovascular system, lungs, and liver. However, their specific relationship with airway fibrosis in COPD has not yet been thoroughly investigated. This study aims to evaluate the concentrations of U-II and TGF-β in individuals with COPD, as well as in healthy smokers and non-smokers, to explore their potential roles in COPD-related fibrosis. The study included three distinct groups: a healthy non-smoker control group (n = 98), a healthy smoker group (n = 78), and a COPD group (n = 80). All participants in the COPD group had a smoking history of at least 10 pack-years. COPD was defined according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines, with only patients classified as GOLD stage 2 or higher being included in the study. Urotensin-II (U-II) and transforming growth factor-β (TGF-β) levels were measured using a commercially available ELISA kit. COPD patients had a significantly lower FEV (58 ± 15.4%) compared to smokers (79 ± 4.5%) and non-smokers (92 ± 3.7%) ( < 0.001). Similarly, COPD patients had a lower FEV/FVC ratio (55 ± 9.4%) compared to smokers (72 ± 4.2%) and non-smokers (85 ± 3.6%) ( < 0.01 and < 0.05, respectively). SaO was significantly lower in COPD patients (87%) compared to smokers (96.5%) and non-smokers (98%) (COPD vs. smokers: < 0.05 and smokers vs. non-smokers: > 0.05). U-II levels were significantly higher in COPD patients (175.10 ± 62.40 pg/mL) compared to smokers (118.50 ± 45.51 pg/mL) and non-smokers (85.29 ± 35.87 pg/mL) ( < 0.001 and < 0.05, respectively). COPD patients also had significantly higher levels of TGF-β (284.60 ± 60.50 pg/mL) compared to smokers (160.00 ± 41.80 pg/mL) and non-smokers (92.00 ± 25.00 pg/mL) ( < 0.001 and < 0.05, respectively). Our study supports the growing body of evidence that U-II and TGF-β play central roles in the development and progression of fibrosis in COPD. The negative correlation between these markers and lung function parameters such as FEV and FEV/FVC indicates that they may be key drivers of airway remodeling and obstruction. These biomarkers could serve as early indicators of fibrotic changes in smokers, even before the onset of COPD.
小气道纤维化在慢性阻塞性肺疾病（COPD）的进展中起着关键作用。先前的研究表明，尾加压素-II（U-II）和转化生长因子-β（TGF-β）可能在包括心血管系统、肺和肝在内的各种器官的病理性纤维化中发挥作用。然而，它们与 COPD 相关气道纤维化的确切关系尚未得到充分研究。本研究旨在评估 COPD 患者以及健康吸烟者和非吸烟者体内 U-II 和 TGF-β 的浓度，以探讨它们在 COPD 相关纤维化中的潜在作用。
健康非吸烟者对照组（n=98）、健康吸烟者组（n=78）和 COPD 组（n=80）。所有 COPD 组患者均有至少 10 包年的吸烟史。COPD 按照全球慢性阻塞性肺疾病倡议（GOLD）指南定义，仅纳入 GOLD 分期 2 或更高的患者。使用商业可得的 ELISA 试剂盒测量尾加压素-II（U-II）和转化生长因子-β（TGF-β）的水平。
COPD 患者的 FEV（58±15.4%）明显低于吸烟者（79±4.5%）和非吸烟者（92±3.7%）（<0.001）。同样，COPD 患者的 FEV/FVC 比值（55±9.4%）也明显低于吸烟者（72±4.2%）和非吸烟者（85±3.6%）（<0.01 和 <0.05，分别）。COPD 患者的 SaO（87%）明显低于吸烟者（96.5%）和非吸烟者（98%）（COPD 与吸烟者：<0.05 和吸烟者与非吸烟者：>0.05）。U-II 水平在 COPD 患者（175.10±62.40 pg/mL）中明显高于吸烟者（118.50±45.51 pg/mL）和非吸烟者（85.29±35.87 pg/mL）（<0.001 和 <0.05，分别）。COPD 患者的 TGF-β（284.60±60.50 pg/mL）水平也明显高于吸烟者（160.00±41.80 pg/mL）和非吸烟者（92.00±25.00 pg/mL）（<0.001 和 <0.05，分别）。
我们的研究支持越来越多的证据表明，U-II 和 TGF-β 在 COPD 纤维化的发展和进展中起着核心作用。这些标志物与肺功能参数（如 FEV 和 FEV/FVC）之间的负相关表明，它们可能是气道重塑和阻塞的关键驱动因素。这些生物标志物可以作为吸烟者纤维化变化的早期指标，甚至在 COPD 发病之前。
