Xia Shijin, Zhou Changxi, Kalionis Bill, Shuang Xiaoping, Ge Haiyan, Gao Wen
1Shanghai Institute of Geriatrics, Huadong Hospital, Fudan University, Shanghai, China.
2Department of Respiratory Medicine, The Second Medical Center of PLA General Hospital, Beijing, China.
Aging Dis. 2020 Feb 1;11(1):129-140. doi: 10.14336/AD.2019.0508. eCollection 2020 Feb.
Chronic Obstructive Pulmonary Disease (COPD) is a worldwide health problem associated with high morbidity and mortality, especially in elderly patients. Aging functions include mitochondrial dysfunction, cell-to-cell information exchange, protein homeostasis and extracellular matrix dysregulation, which are closely related to chronic inflammatory response and oxidation-antioxidant imbalance in the pathogenesis of COPD. COPD displays distinct inflammaging features, including increased cellular senescence and oxidative stress, stem cell exhaustion, alterations in the extracellular matrix, reduced levels of endogenous anti-inflammaging molecules, and reduced autophagy. Given that COPD and inflammaging share similar general features, it is very important to identify the specific mechanisms of inflammaging, which involve oxidative stress, inflammation and lung mesenchymal stem cell function in the development of COPD, especially in elderly COPD patients. In this review, we highlight the studies relevant to COPD progression, and focus on mechanisms associated with inflammaging.
慢性阻塞性肺疾病（COPD）是一个全球性的健康问题，发病率和死亡率都很高，尤其是在老年患者中。衰老的功能包括线粒体功能障碍、细胞间信息交换、蛋白质稳态和细胞外基质失调，这些与COPD发病机制中的慢性炎症反应和氧化-抗氧化失衡密切相关。COPD表现出明显的炎症衰老特征，包括细胞衰老和氧化应激增加、干细胞耗竭、细胞外基质改变、内源性抗炎症衰老分子水平降低以及自噬减少。鉴于COPD和炎症衰老具有相似的一般特征，识别炎症衰老的具体机制非常重要，这些机制涉及氧化应激、炎症和肺间充质干细胞功能在COPD发展中的作用，尤其是在老年COPD患者中。在这篇综述中，我们重点介绍了与COPD进展相关的研究，并关注与炎症衰老相关的机制。
