Tobacco Smoke-Induced Lung Fibrosis and Emphysema

被引:64
|
作者
Morse, Danielle [1 ]
Rosas, Ivan O. [1 ,2 ]
机构
[1] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Pulm & Crit Care, Boston, MA 02115 USA
[2] Lovelace Resp Res Inst, Pulm Fibrosis Program, Albuquerque, NM 87108 USA
来源
ANNUAL REVIEW OF PHYSIOLOGY, VOL 76 | 2014年 / 76卷
关键词
COPD; IPF; senescence; autophagy; TGF-beta; inflammasome; IDIOPATHIC-PULMONARY-FIBROSIS; ENDOPLASMIC-RETICULUM STRESS; MUC5B PROMOTER POLYMORPHISM; GENOME-WIDE ASSOCIATION; CIGARETTE-SMOKE; DNA-DAMAGE; OXIDATIVE STRESS; INTERSTITIAL PNEUMONIA; MOLECULAR-MECHANISMS; MAMMALIAN AUTOPHAGY;
D O I
10.1146/annurev-physiol-021113-170411
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Despite public health campaigns discouraging smoking, 1,000 American children every day become smokers, ensuring that tobacco-related health complications will be with us for decades to come. Smoking is the greatest risk factor for both chronic obstructive lung disease and interstitial lung disease. The facts that not every smoker develops chronic lung disease and that lung pathology differs markedly among smokers indicate that individual susceptibility must be a central determinant of lung injury responses to cigarette smoke. Comparative examination of pathogenic mechanisms of smoke-induced lung disease can shed light on the homeostatic pathways critical to maintaining lung health. In this review, we explore common and divergent biological forces tilting the lung homeostatic balance away from health and toward emphysema or pulmonary fibrosis. We emphasize recent insights that highlight the greatest contrasts or similarities in the pathogenesis of these two chronic lung disease phenotypes.
引用
收藏
页码:493 / 513
页数:21
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