Welcome to the Rahman Lab
My laboratory is interested in understanding the redox signaling, mechanism of proinflammatory gene expression by studying the chromatin remodeling-epigenetic changes (histone acetylation/deacetylation and DNA methylation), involvement of anti-inflammatory and anti-aging proteins sirtuins, HDACs, DNA damage/repair, and cellular senescence in chronic lung inflammatory diseases including COPD. Recent research includes in understanding the role of sirtuins/HDACs in aging and accelerated decline in lung function, cellular senescence, and regulation of circadian genes. Our long-term goal is to understand the cellular and molecular mechanisms involved in the pathogenesis of chronic inflammatory lung diseases caused by environmental toxicants (tobacco smoke, e-cigarettes, oxidants/aldehydes), identifying molecular targets, and the potential benefit of therapeutic interventions in airways disease.
Current Research Projects
Inflammation, Advancing Age and Nutrition, 1st Edition
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- Impaired mitophagy leads to cigarette smoke stress-induced cellular senescence: Implications for chronic obstructive pulmonary disease. FASEB J. In press. (2015 Mar 19).
- Environmental health hazards of e-cigarettes and their components: Oxidants and copper in e-cigarette aerosols. Environ Pollut. 198, 100-7. (2015 Mar 01).
- Vapors produced by electronic cigarettes and e-juices with flavorings induce toxicity, oxidative stress, and inflammatory response in lung epithelial cells and in mouse lung. PLoS One. 10, e0116732. (2015 Jan 01).