School of Medicine, Trinity Biomedical Sciences Institute, Trinity College Dublin, Ireland.
Division of Pulmonary and Critical Care Medicine, Joan and Sanford I. Weill Department of Medicine, New York, NY, U.S.A.
Clin Sci (Lond). 2023 Feb 14;137(3):219-237. doi: 10.1042/CS20210504.
Chronic obstructive pulmonary disease (COPD) is a debilitating lung disease characterised by airflow limitation, chronic bronchitis, emphysema and airway remodelling. Cigarette smoke is considered the primary risk factor for the development of COPD; however, genetic factors, host responses and infection also play an important role. Accumulating evidence highlights a role for iron dyshomeostasis and cellular iron accumulation in the lung as a key contributing factor in the development and pathogenesis of COPD. Recent studies have also shown that mitochondria, the central players in cellular iron utilisation, are dysfunctional in respiratory cells in individuals with COPD, with alterations in mitochondrial bioenergetics and dynamics driving disease progression. Understanding the molecular mechanisms underlying the dysfunction of mitochondria and cellular iron metabolism in the lung may unveil potential novel investigational avenues and therapeutic targets to aid in the treatment of COPD.
慢性阻塞性肺疾病（COPD）是一种使人虚弱的肺部疾病，其特征是气流受限、慢性支气管炎、肺气肿和气道重塑。香烟烟雾被认为是 COPD 发展的主要危险因素；然而，遗传因素、宿主反应和感染也起着重要作用。越来越多的证据强调了铁动态平衡和细胞内铁积累在肺部作为 COPD 发展和发病机制的关键因素的作用。最近的研究还表明，线粒体作为细胞内铁利用的核心参与者，在 COPD 患者的呼吸细胞中功能失调，线粒体生物能学和动力学的改变推动了疾病的进展。了解肺线粒体功能障碍和细胞内铁代谢的分子机制可能揭示潜在的新的研究途径和治疗靶点，以帮助治疗 COPD。
