Please use this identifier to cite or link to this item: https://doi.org/10.1007/s11882-012-0328-6
Title: Gene expression signatures: A new approach to understanding the pathophysiology of chronic rhinosinusitis
Authors: Li, C. 
Shi, L.
Yan, Y.
Gordon, B.R.
Gordon, W.M.
Wang, D.-Y.
Keywords: Chronic rhinosinusitis (CRS)
Environmental factors
Gene expression signatures
Glucocorticosteroids
Host defense mechanisms
Inflammation
Nasal epithelium
Nasal polyps
Pathophysiology
Regulatory T cells (T-reg)
Remodeling
Issue Date: Apr-2013
Citation: Li, C., Shi, L., Yan, Y., Gordon, B.R., Gordon, W.M., Wang, D.-Y. (2013-04). Gene expression signatures: A new approach to understanding the pathophysiology of chronic rhinosinusitis. Current Allergy and Asthma Reports 13 (2) : 209-217. ScholarBank@NUS Repository. https://doi.org/10.1007/s11882-012-0328-6
Abstract: Chronic rhinosinusitis (CRS) is a complex inflammatory disease with variable disease manifestation. Though external risk factors are associated with development and/or persistence of CRS, the host mucosal response is also important, as nasal epithelium acts as a physical and immune barrier. Under inflammatory stress, the nasal epithelium can undergo injury, followed by a rapid remodeling response ranging from epithelial hyperplasia, to goblet-cell metaplasia, to denudation, loss of cilia, fibrosis, and basement membrane thickening. Identification of gene expression signatures and molecular pathways in CRS pathogenesis have now begun to contribute significantly to a better understanding of the genetic and molecular alterations underlying CRS development and progression. Genetic studies are especially illuminating when multiple gene variants synergize within a permissive environmental context, and are expected to guide development of more effective therapeutic targets for CRS treatment. © 2012 Springer Science+Business Media New York.
Source Title: Current Allergy and Asthma Reports
URI: http://scholarbank.nus.edu.sg/handle/10635/109360
ISSN: 15297322
DOI: 10.1007/s11882-012-0328-6
Appears in Collections:Staff Publications

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