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Senescence in COPD and Its Comorbidities
Annual Review of Physiology ( IF 18.2 ) Pub Date : 2017-02-13 00:00:00 , DOI: 10.1146/annurev-physiol-022516-034314
Peter J. Barnes 1
Affiliation  

Chronic obstructive pulmonary disease (COPD) is regarded as a disease of accelerated lung aging. This affliction shows all of the hallmarks of aging, including telomere shortening, cellular senescence, activation of PI3 kinase-mTOR signaling, impaired autophagy, mitochondrial dysfunction, stem cell exhaustion, epigenetic changes, abnormal microRNA profiles, immunosenescence, and a low-grade chronic inflammation (inflammaging). Many of these pathways are driven by chronic exogenous and endogenous oxidative stress. There is also a reduction in antiaging molecules, such as sirtuins and Klotho, which further accelerate the aging process. COPD is associated with several comorbidities (multimorbidity), such as cardiovascular and metabolic diseases, that share the same pathways of accelerated aging. Understanding these mechanisms has helped identify several novel therapeutic targets, and several drugs and dietary interventions are now in development to treat multimorbidity.

中文翻译:


慢性阻塞性肺病的衰老及其合并症

慢性阻塞性肺疾病(COPD)被认为是加速肺衰老的疾病。这种痛苦显示出所有衰老的特征,包括端粒缩短,细胞衰老,PI3激酶-mTOR信号激活,自噬受损,线粒体功能障碍,干细胞衰竭,表观遗传变化,微小RNA谱,免疫衰老和低度慢性炎症(发炎)。这些途径中的许多是由慢性外源性和内源性氧化应激驱动的。抗衰老分子(例如sirtuins和Klotho)的减少也进一步加速了衰老过程。COPD与多种合并症(多发病)相关,例如心血管疾病和代谢性疾病,它们具有加速衰老的相同途径。

更新日期:2017-02-13
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