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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- SIRT1 protects against cigarette smoke-induced lung oxidative stress via a FOXO3-dependent mechanism. Am J Physiol Lung Cell Mol Physiol. 306, L816-28. (2014 May 01).
- Cigarette smoke induces distinct histone modifications in lung cells: implications for the pathogenesis of COPD and lung cancer. J Proteome Res. 13, 982-96. (2014 Feb 07).
- Nrf2 reduces levels of phosphorylated tau protein by inducing autophagy adaptor protein NDP52. Nat Commun. 5, 3496. (2014 Jan 01).