Szalontai Klára, Gémes Nikolett, Furák József, Varga Tünde, Neuperger Patrícia, Balog József Á, Puskás László G, Szebeni Gábor J
Csongrád County Hospital of Chest Diseases, Alkotmány u. 36., H6772 Deszk, Hungary.
Laboratory of Functional Genomics, Biological Research Centre, Temesvári krt. 62., H6726 Szeged, Hungary.
J Clin Med. 2021 Jun 29;10(13):2889. doi: 10.3390/jcm10132889.
Chronic obstructive pulmonary disease (COPD), the frequently fatal pathology of the respiratory tract, accounts for half a billion cases globally. COPD manifests via chronic inflammatory response to irritants, frequently to tobacco smoke. The progression of COPD from early onset to advanced disease leads to the loss of the alveolar wall, pulmonary hypertension, and fibrosis of the respiratory epithelium. Here, we focus on the epidemiology, progression, and biomarkers of COPD with a particular connection to lung cancer. Dissecting the cellular and molecular players in the progression of the disease, we aim to shed light on the role of smoking, which is responsible for the disease, or at least for the more severe symptoms and worse patient outcomes. We summarize the inflammatory conditions, as well as the role of EMT and fibroblasts in establishing a cancer-prone microenvironment, i.e., the soil for 'COPD-derived' lung cancer. We highlight that the major health problem of COPD can be alleviated via smoking cessation, early diagnosis, and abandonment of the usage of biomass fuels on a global basis.
慢性阻塞性肺疾病(COPD)是一种常见的致命呼吸道疾病,全球病例数达5亿。COPD通过对刺激物(通常是烟草烟雾)的慢性炎症反应表现出来。COPD从早期发病发展到晚期疾病会导致肺泡壁丧失、肺动脉高压和呼吸道上皮纤维化。在这里,我们重点关注COPD的流行病学、进展和生物标志物,特别是与肺癌的关联。通过剖析疾病进展中的细胞和分子因素,我们旨在阐明吸烟的作用,吸烟是导致该疾病的原因,或者至少是导致更严重症状和更差患者预后的原因。我们总结了炎症状况,以及上皮-间质转化(EMT)和成纤维细胞在建立易患癌症的微环境(即“COPD衍生”肺癌的土壤)中的作用。我们强调,通过戒烟、早期诊断以及在全球范围内放弃使用生物质燃料,可以缓解COPD的主要健康问题。