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Biomed J. 2015 Mar-Apr;38(2):117-24. doi: 10.4103/2319-4170.143478.

Genomic instability in chronic airway inflammatory diseases.

Author information

1
Department of Respiratory and Critical Care Medicine, Second Affiliated Hospital, Institute of Respiratory Diseases, Zhejiang University School of Medicine, Hangzhou; State Key Lab for Respiratory Diseases, Guangzhou, China.
2
Department of Pharmacology; Department of Respiratory and Critical Care Medicine, Second Affiliated Hospital, Institute of Respiratory Diseases, Zhejiang University School of Medicine, Hangzhou, China.

Abstract

Chronic airway inflammatory diseases are life-threatening conditions, including bronchial asthma, chronic obstructive pulmonary disease (COPD), and so on. However, as the disease etiology remains largely unclear, current treatments that target chronic airway inflammatory diseases are still not satisfactory. DNA damage response (DDR), regarded as one of the many causes of apoptosis and cell senescence, as well as a factor involved in carcinogenesis, has recently begun to attract attention as a source of chronic inflammation. Considering that COPD and allergic asthma inflammation enhance DNA damage, measures related with DNA repair should be taken so as to reduce the injuries caused by these airway diseases. Small molecule inhibitors specifically against various DNA repair proteins have been developed over the last decade to fight against chronic diseases. Poly(ADP-ribose) polymerase (PARP) inhibitor, for example, has already shown its potential in asthma animal models to block airway inflammation. In this review, we highlight the roles of DDR in chronic airway inflammatory diseases, and try to have a better understanding of these diseases. We also discuss the possibilities of targeting DDR signaling to develop potential novel treatments against these conditions.

PMID:
25355386
DOI:
10.4103/2319-4170.143478
[Indexed for MEDLINE]
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