Oxidant and cigarette smoke-mediated lung inflammation.
Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation that is not fully reversible. It is a disabling condition associated with progressive breathlessness. COPD will account for over 6 million deaths per year in 2020 (3rd major cause of death), and move from the sixth- to the third-leading cause of death worldwide. In America, COPD affects 9% of residents aged 60 years and above and it ranked fourth in the recent morbidity survey of the elderly population. It is estimated that approximately 23.4 million people in the US have COPD and the health burden is $36.1 billions per year. At present, there is no effective treatment exists to halt the decline in lung function in response to smoking. This in turn reflects a lack of understanding of the specific cellular and molecular pathways triggered in the lung by tobacco smoke/oxidants.
Our laboratory is interested in understanding the redox signaling, mechanism of proinflammatory gene expression by studying the chromatin remodeling-epigenetic changes (histone acetylation/deacetylation) on pro-inflammatory genes, involvement of anti-inflammatory and anti-aging proteins sirtuins, and steroid resistance in chronic inflammatory diseases/COPD. Recent research includes in understanding the role of sirtuins in aging and accelerated decline in lung function and regulation of circadian genes. Our long-term goal is to understand the cellular and molecular mechanisms involved in pathogenesis of COPD, and the potential benefit of therapeutic interventions in this debilitating disease.