Current concepts on the role of inflammation in COPD and lung cancer.

Current concepts on the role of inflammation in COPD and lung cancer.
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DOI:
10.1016/j.coph.2009.06.009
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发表时间:
2009-08
影响因子:
4
通讯作者:
Rahman, Irfan
Rahman, Irfan
中科院分区:
医学3区
文献类型:
--
作者:
Yao, Hongwei;Rahman, Irfan

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慢性阻塞性肺疾病(COPD)和肺癌是导致死亡的主要原因,两者都与吸烟有关。已经显示,50-70%的诊断为肺癌的患者患有COPD,并且肺功能降低是肺癌中的重要事件,表明COPD和肺癌之间的关联。然而,COPD和肺肿瘤发生之间的因果关系尚未完全了解。最近的研究表明,慢性炎症在这两种疾病的发病机制中起着核心作用。例如,免疫功能障碍、NF-κB的异常激活、上皮-间质转化、改变的粘附信号传导途径和细胞外基质降解/改变的信号传导是COPD和肺癌的关键潜在机制。这些参数沿着其他过程,如染色质修饰/表观遗传变化、血管生成和自噬/凋亡被香烟烟雾改变,在COPD和肺癌的发展中至关重要。了解这些过程背后的细胞和分子机制将为阻止COPD的慢性炎症和制定肺癌的治疗策略提供新的途径。
Chronic obstructive pulmonary disease (COPD) and lung cancer are leading cause of death, and both are associated with cigarette smoke exposure. It has been shown that 50–70% of patients diagnosed with lung cancer suffer from COPD, and reduced lung function is an important event in lung cancer suggesting an association between COPD and lung cancer. However, a causal relationship between COPD and lung tumorigenesis is not yet fully understood. Recent studies have suggested a central role of chronic inflammation in pathogenesis of both the diseases. For example, immune dysfunction, abnormal activation of NF-κB, epithelial-to-mesenchymal transition, altered adhesion signaling pathways, and extracellular matrix degradation/altered signaling are the key underlying mechanisms in both COPD and lung cancer. These parameters along with other processes, such as chromatin modifications/epigenetic changes, angiogenesis, and autophagy/apoptosis are altered by cigarette smoke, are crucial in the development of COPD and lung cancer. Understanding the cellular and molecular mechanisms underlying these processes will provide novel avenues for halting the chronic inflammation in COPD and devising therapeutic strategies against lung cancer.
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