期刊
AUTOPHAGY
卷 14, 期 2, 页码 221-232出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2017.1389823
关键词
asthma; autophagy; chronic obstructive pulmonary disease (COPD); inflammation; pulmonary fibrosis; pulmonary hypertension; sleep apnea; tuberculosis
类别
资金
- American Lung Association of the Northeast [RG-348928]
- HHS \ NIH \ National Heart, Lung, and Blood Institute (NHBLI) [P01-HL114501, R01-HL079904, P01-HL105339, K99-HL125899, R01-HL055330]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [K99HL125899, R00HL125899, R01HL132198, T32HL134629] Funding Source: NIH RePORTER
Persistent inflammation within the respiratory tract underlies the pathogenesis of numerous chronic pulmonary diseases including chronic obstructive pulmonary disease, asthma and pulmonary fibrosis. Chronic inflammation in the lung may arise from a combination of genetic susceptibility and environmental influences, including exposure to microbes, particles from the atmosphere, irritants, pollutants, allergens, and toxic molecules. To this end, an immediate, strong, and highly regulated inflammatory defense mechanism is needed for the successful maintenance of homeostasis within the respiratory system. Macroautophagy/autophagy plays an essential role in the inflammatory response of the lung to infection and stress. At baseline, autophagy may be critical for inhibiting spontaneous pulmonary inflammation and fundamental for the response of pulmonary leukocytes to infection; however, when not regulated, persistent or inefficient autophagy may be detrimental to lung epithelial cells, promoting lung injury. This perspective will discuss the role of autophagy in driving and regulating inflammatory responses of the lung in chronic lung diseases with a focus on potential avenues for therapeutic targeting.
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