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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- Electronic cigarette aerosols and copper nanoparticles induce mitochondrial stress and promote DNA fragmentation in lung fibroblasts.Biochem Biophys Res Commun. 477, 620-5. (2016 Sep 02).
- Shelterin TPP1 Reduction Causes Telomere Attrition and Cellular Senescence via Sirt1 Deacetylase in Chronic Obstructive Pulmonary Disease.Am J Respir Cell Mol Biol. (2016 Aug 25).
- Mitochondrial redox system, dynamics, and dysfunction in lung inflammaging and COPD.Int J Biochem Cell Biol, . (2016 Jul 26).