Is the aging process accelerated in chronic obstructive pulmonary disease?
Is the aging process accelerated in chronic obstructive pulmonary disease?
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DOI：
10.1097/mcp.0b013e328341cead
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发表时间：
2011-03-01
影响因子：
3.3
通讯作者：
Sin, Don D.
中科院分区：
文献类型：
--
作者：
Lee, Jee;Sandford, Andrew;Sin, Don D.
综述目的最近的研究表明，慢性阻塞性肺疾病(COPD)可能是一种加速衰老的疾病。COPD发病机制的衰老假说得到了体外、体内和临床研究的支持。这篇综述的目的是全面综述COPD的衰老假说，并总结用于评估细胞衰老的方法。最近的发现暴露于香烟烟雾中导致的加速衰老被认为是导致COPD快速进展的假说。最近的研究表明，与健康对照组相比，COPD患者肺和外周循环中衰老相关蛋白的表达增强。加速衰老的小鼠模型显示肺内出现自发的肺气肿改变，而COPD患者的肺显示成纤维细胞和肺泡细胞中衰老的标记增强。最近，对端粒的研究表明，与健康对照组相比，COPD患者可能会经历更快的端粒磨损。端粒随着细胞老化而缩短。然而，到目前为止，研究相对较少，并且产生了不同的结果。摘要：加速衰老在COPD进展中的作用的证据正在增加，衰老是COPD发生的一种可能的分子途径。
Purpose of reviewRecent research suggests that chronic obstructive pulmonary disease (COPD) may be a disease of accelerated aging. The senescence hypothesis of COPD pathogenesis is supported by in-vitro, in-vivo and clinical studies. The purpose of this review is to provide a comprehensive overview of the senescence hypothesis of COPD and summarize methods that are used to assess cellular aging.Recent findingsAccelerated aging due to exposure to cigarette smoke is hypothesized to induce rapid progression of COPD. Recent studies have shown that COPD patients have enhanced expression of senescence-associated proteins in the lung and in the peripheral circulation compared to healthy controls. Murine models of accelerated aging demonstrate spontaneous emphysematous changes in the lungs, while lungs of COPD patients demonstrate enhanced markers of senescence in fibroblasts and alveolar cells. More recently, studies of telomeres, which shorten with cellular aging, have shown that COPD patients may experience accelerated telomere attrition compared with healthy controls. However, studies to date have been relatively small and have produced heterogeneous results.SummaryThe evidence for the role of accelerated aging in COPD progression is growing and senescence is one possible molecular pathway by which COPD occurs.