Targeting Aging Pathways in Chronic Obstructive Pulmonary Disease

被引:93
作者
Easter, Molly [1 ]
Bollenbecker, Seth [1 ]
Barnes, Jarrod W. [1 ,2 ]
Krick, Stefanie [1 ,2 ]
机构
[1] Univ Alabama Birmingham, Div Pulm Allergy & Crit Care Med, Dept Med, Birmingham, AL 35294 USA
[2] Univ Alabama Birmingham, Gregory Fleming James Cyst Fibrosis Ctr, Birmingham, AL 35294 USA
关键词
COPD; aging; senescence; inflammation; senolytics; cigarette smoke; VOLUME-REDUCTION SURGERY; BLOOD EOSINOPHIL COUNT; LIFE-SPAN; CELLULAR SENESCENCE; OXIDATIVE STRESS; CIGARETTE-SMOKE; GROWTH-FACTOR; STEM-CELLS; DROSOPHILA-MELANOGASTER; LUNG TRANSPLANTATION;
D O I
10.3390/ijms21186924
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Chronic obstructive pulmonary disease (COPD) has become a global epidemic and is the third leading cause of death worldwide. COPD is characterized by chronic airway inflammation, loss of alveolar-capillary units, and progressive decline in lung function. Major risk factors for COPD are cigarette smoking and aging. COPD-associated pathomechanisms include multiple aging pathways such as telomere attrition, epigenetic alterations, altered nutrient sensing, mitochondrial dysfunction, cell senescence, stem cell exhaustion and chronic inflammation. In this review, we will highlight the current literature that focuses on the role of age and aging-associated signaling pathways as well as their impact on current treatment strategies in the pathogenesis of COPD. Furthermore, we will discuss established and experimental COPD treatments including senolytic and anti-aging therapies and their potential use as novel treatment strategies in COPD.
引用
收藏
页码:1 / 17
页数:17
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