Cellular senescence in normal and premature lung aging

被引:4
作者
Bartling, B. [1 ]
机构
[1] Univ Klinikum Halle Saale AoR, Klin & Poliklin Herz & Thoraxchirurg, D-06120 Halle, Saale, Germany
来源
ZEITSCHRIFT FUR GERONTOLOGIE UND GERIATRIE | 2013年 / 46卷 / 07期
关键词
Cellular senescence; Lung; Aging; Pulmonary disease; Smoking; OBSTRUCTIVE PULMONARY-DISEASE; ALVEOLAR EPITHELIAL-CELLS; DNA-DAMAGE RESPONSE; TOBACCO-SMOKE; IN-VITRO; H2AX PHOSPHORYLATION; TELOMERASE ACTIVITY; DOWN-REGULATION; EMPHYSEMA SHOW; A549; CELLS;
D O I
10.1007/s00391-013-0543-3
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
The incidence of chronic respiratory diseases (e.g., chronic obstructive pulmonary disease, COPD) and interstitial lung diseases (e.g., pneumonia and lung fibrosis) increases with age. In addition to immune senescence, the accumulation of senescent cells directly in lung tissue might play a critical role in the increased prevalence of these pulmonary diseases. In the last couple of years, detailed studies have identified the presence of senescent cells in the aging lung and in diseased lungs of patients with COPD and lung fibrosis. Cellular senescence has been shown for epithelial cells of bronchi and alveoli as well as mesenchymal and vascular cells. Known risk factors for pulmonary diseases (cigarette smoke, air pollutions, bacterial infections, etc.) were identified in experimental studies as being possible mediators in the development of cellular senescence. The present findings indicate the importance of cellular senescence in normal lung aging and in premature aging of the lung in patients with COPD, lung fibrosis, and probably other respiratory diseases.
引用
收藏
页码:613 / +
页数:9
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