Journal
BIOCHEMICAL SOCIETY TRANSACTIONS
Volume 35, Issue -, Pages 1151-1155Publisher
PORTLAND PRESS LTD
DOI: 10.1042/BST0351151
Keywords
chronic obstructive pulmonary disease (COPD); cigarette smoke; histone deacetylase (HDAC); Nox; nuclear factor-erythroid 2 p45 subunit-related factor 2 (Nrf2); oxidant
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Regulation of reduction/oxidation (redox) state is critical for cell viability, activation, proliferation and organ function, and imbalance of oxidant/antioxidant balance is implicated in various chronic respiratory inflammatory diseases, such as asthma, pulmonary fibrosis and chronic obstructive pulmonary disease. CS (cigarette smoke) is a complex mixture of various noxious gases and condensed tar particles. These components elicit oxidative stress in lungs by continuous generation of ROS (reactive oxygen species) and various inflammatory mediators. in the present review, we have discussed the role of oxidative stress in triggering the inflammatory response in the lungs in response to CS by demonstrating the role of NADPH oxidase, redox-sensitive transcription factors, such as pro-inflammatory NF-kappa B (nuclear factor kappa B) and antioxidant Nrf2 (nuclear factor-erythroid 2 p45 subunit-related factor 2), as well as HDAC (histone deacetylase) in pro-inflammatory cytokine release by disruption of HDAC-RelA/p65 NF-kappa B complex.
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