Genomics of Otitis Media (OM): Molecular Genetics Approaches to Characterize Disease Pathophysiology
Otitis media (OM) is an infective and inflammatory disorder known to be a major cause of hearing impairment across all age groups. Both acute and chronic OM result in substantial healthcare utilization related to antibiotic prescription and surgical procedures necessary for its management. Although...
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Published in | Frontiers in genetics Vol. 11; p. 313 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Switzerland
Frontiers Media S.A
23.04.2020
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Subjects | |
Online Access | Get full text |
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Summary: | Otitis media (OM) is an infective and inflammatory disorder known to be a major cause of hearing impairment across all age groups. Both acute and chronic OM result in substantial healthcare utilization related to antibiotic prescription and surgical procedures necessary for its management. Although several studies provided evidence of genetics playing a significant role in the susceptibility to OM, we had limited knowledge about the genes associated with OM until recently. Here we have summarized the known genetic factors that confer susceptibility to various forms of OM in mice and in humans and their genetic load, along with associated cellular signaling pathways. Spotlighted in this review are fucosyltransferase (FUT) enzymes, which have been implicated in the pathogenesis of OM. A comprehensive understanding of the functions of OM-associated genes may provide potential opportunities for its diagnosis and treatment. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 These authors have contributed equally to this work This article was submitted to Genetic Disorders, a section of the journal Frontiers in Genetics Reviewed by: Lena Hafren, University of Helsinki, Finland; Gijs Van Ingen, Erasmus Medical Center, Netherlands Edited by: Regie Santos-Cortez, University of Colorado, United States |
ISSN: | 1664-8021 1664-8021 |
DOI: | 10.3389/fgene.2020.00313 |