Yoshida Toshinori, Tuder Rubin M
Division of Cardiopulmonary Pathology, Department of Pathology, School of Medicine, Johns Hopkins University, Baltimore, Maryland 21205, USA.
Physiol Rev. 2007 Jul;87(3):1047-82. doi: 10.1152/physrev.00048.2006.
Chronic obstructive pulmonary diseases (COPD), comprised of pulmonary emphysema, chronic bronchitis, and structural and inflammatory changes of small airways, is a leading cause of morbidity and mortality in the world. A better understanding of the pathobiology of COPD is critical for the developing of novel therapies, as the majority of patients with the disease have little therapeutic options at the present time. The pathobiology of COPD encompasses multiple injurious processes including inflammation (excessive or inappropriate innate and adaptive immunity), cellular apoptosis, altered cellular and molecular alveolar maintenance program, abnormal cell repair, extracellular matrix destruction (protease and anti-protease imbalance), and oxidative stress (oxidant and antioxidant imbalance). These processes are triggered by urban and rural air pollutants and active and/or passive cigarette smoke and modified by cellular senescence and infection. A series of receptor-mediated signal transduction pathways are activated by reactive oxygen species and tobacco components, resulting in impairment of a variety of cell signaling and cytokine networks, subsequently leading to chronic airway responses with mucus production, airway remodeling, and alveolar destruction. The authors provide an updated insight into the molecular and cellular pathobiology of COPD based on human and/or animal data.
慢性阻塞性肺疾病（COPD）包括肺气肿、慢性支气管炎以及小气道的结构和炎症变化，是全球发病和死亡的主要原因。更好地理解COPD的病理生物学对于开发新疗法至关重要，因为目前大多数该疾病患者几乎没有治疗选择。COPD的病理生物学包括多种损伤过程，包括炎症（过度或不适当的固有免疫和适应性免疫）、细胞凋亡、细胞和分子肺泡维持程序改变、异常细胞修复、细胞外基质破坏（蛋白酶和抗蛋白酶失衡）以及氧化应激（氧化剂和抗氧化剂失衡）。这些过程由城乡空气污染物以及主动和/或被动吸烟引发，并受细胞衰老和感染影响。一系列受体介导的信号转导途径被活性氧和烟草成分激活，导致各种细胞信号传导和细胞因子网络受损，随后导致伴有黏液产生、气道重塑和肺泡破坏的慢性气道反应。作者基于人类和/或动物数据，对COPD的分子和细胞病理生物学提供了最新见解。
