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2026年8月26日星期三
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吸烟者之肺:何去何从?——探索肺气肿、肺癌与纤维化中共享及特有的吸烟相关分子通路(阐述性综述)

Smoker's Lungs: Quo Vadis? Exploring the Shared and Individual Smoking-Related Molecular Pathways of Emphysema, Carcinoma, and Fibrosis - An Illustrative Review.

期刊
Thoracic Cancer
PMID
42639684
原文
PubMed ↗
发布日期

作者

  • Lovorka Grgurević — Department of Anatomy, "Drago Perović", School of Medicine, University of Zagreb, Zagreb, Croatia.
  • Stela Hrkač — Department of Clinical Immunology, Allergology and Rheumatology, University Hospital Dubrava, Zagreb, Croatia.
  • Ruđer Novak — Department of Proteomics, Center for Translational and Clinical Research, School of Medicine, University of Zagreb, Zagreb, Croatia.
  • Grgur Salai — Department of Pulmonology, University Hospital Dubrava, Zagreb, Croatia.
  • Joško Mitrović — Department of Clinical Immunology, Allergology and Rheumatology, University Hospital Dubrava, Zagreb, Croatia.
  • Tomo Svaguša — Department of Cardiovascular Disease, University Hospital Dubrava, Zagreb, Croatia.

作者单位

  • Department of Anatomy, "Drago Perović", School of Medicine, University of Zagreb, Zagreb, Croatia.
  • Department of Clinical Immunology, Allergology and Rheumatology, University Hospital Dubrava, Zagreb, Croatia.
  • Department of Proteomics, Center for Translational and Clinical Research, School of Medicine, University of Zagreb, Zagreb, Croatia.
  • Department of Pulmonology, University Hospital Dubrava, Zagreb, Croatia.
  • Department of Cardiovascular Disease, University Hospital Dubrava, Zagreb, Croatia.

摘要

中文

吸烟是肺癌和慢性阻塞性肺疾病(COPD)的主要可预防危险因素;此外,吸烟也与特发性肺纤维化(IPF)相关。香烟烟雾主要引起肺部的慢性上皮损伤,在肺微环境内触发一系列相互关联的分子反应。为探索恶性转化(非小细胞肺癌)、肺组织破坏(COPD背景下的肺气肿)和异常愈合(IPF)过程中共同及各自重要的通路,我们进行了一篇叙述性综述,探讨了多种选定过程的作用,包括NFκB活化、线粒体功能障碍、活性氧的作用以及通过Keap1/Nrf2和TGFβ介导的信号传导产生的抗氧化反应,并结合各自疾病的背景。本综述并非旨在作为这些疾病发病机制中病理生理过程的详尽参考,而是旨在说明所选疾病过程之间的共同特征和具体差异。鉴于烟草使用的持续全球负担,进一步研究香烟烟雾暴露的相互关联的分子后果对于推进肺病学的预防和治疗方法仍然至关重要。

English

Cigarette smoking is a major preventable risk factor for the development of lung cancer and chronic obstructive pulmonary disease (COPD); furthermore, it is also associated with idiopathic pulmonary fibrosis (IPF). Cigarette smoke primarily induces chronic epithelial injury in the lungs, initiating a cascade of interconnected molecular responses within the pulmonary microenvironment. Aiming to explore the common and individual important pathways in the processes of malignant alteration (non-small cell carcinoma), lung tissue destruction (emphysema in the context of COPD), and aberrant healing (IPF), we conducted a narrative review in which we explore the roles of various selected processes, including NFκB activation, mitochondrial dysfunction, the role of reactive oxygen species, and the antioxidant response via Keap1/Nrf2 and TGFβ-mediated signaling, in the context of their respective disease. This review is not meant to represent an exhaustive reference of pathophysiologic processes involved in the pathogenesis of these diseases, but to illustrate the common features and specific differences among the selected disease processes. Given the persistent global burden of tobacco use, further research into the interconnected molecular consequences of cigarette smoke exposure remains essential for advancing both preventive and therapeutic approaches in pulmonary medicine.

分类与指标

研究类型
综述Meta
病种
肺癌
JCR 分区
Q2
影响因子
2.6
新锐分区
4区