A novel hypothesis for COVID-19 pathogenesis: Retinol depletion and retinoid signaling disorder

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dc.contributor.authorSarohan, Aziz Rodan
dc.contributor.authorKızıl, Murat
dc.contributor.authorİnkaya, Ahmet Çağkan
dc.contributor.authorMahmud, Shokhan
dc.contributor.authorAkram, Muhammad
dc.contributor.authorCen, Osman
dc.date.accessioned2022-03-09T06:24:15Z
dc.date.available2022-03-09T06:24:15Z
dc.date.issued2021en_US
dc.departmentDicle Üniversitesi, Fen Bilimleri Enstitüsü, Kimya Ana Bilim Dalıen_US
dc.descriptionPMID: 34438017
dc.descriptionWOS:000702705800007
dc.description.abstractThe SARS-CoV-2 virus has caused a worldwide COVID-19 pandemic. In less than a year and a half, more than 200 million people have been infected and more than four million have died. Despite some improvement in the treatment strategies, no definitive treatment protocol has been developed. The pathogenesis of the disease has not been clearly elucidated yet. A clear understanding of its pathogenesis will help develop effective vaccines and drugs. The immunopathogenesis of COVID-19 is characteristic with acute respiratory distress syndrome and multiorgan involvement with impaired Type I interferon response and hyperinflammation. The destructive systemic effects of COVID-19 cannot be explained simply by the viral tropism through the ACE2 and TMPRSS2 receptors. In addition, the recently identified mutations cannot fully explain the defect in all cases of Type I interferon synthesis. We hypothesize that retinol depletion and resulting impaired retinoid signaling play a central role in the COVID-19 pathogenesis that is characteristic for dysregulated immune system, defect in Type I interferon synthesis, severe inflammatory process, and destructive systemic multiorgan involvement. Viral RNA recognition mechanism through RIG-I receptors can quickly consume a large amount of the body's retinoid reserve, which causes the retinol levels to fall below the normal serum levels. This causes retinoid insufficiency and impaired retinoid signaling, which leads to interruption in Type I interferon synthesis and an excessive inflammation. Therefore, reconstitution of the retinoid signaling may prove to be a valid strategy for management of COVID-19 as well for some other chronic, degenerative, inflammatory, and autoimmune diseases.en_US
dc.identifier.citationSarohan, A. D., Kızıl, M., İnkaya, A. Ç., Mahmud, S., Akram, M. ve Cen, O. (2021). A novel hypothesis for COVID-19 pathogenesis: Retinol depletion and retinoid signaling disorder. Cellular Signalling, 87, 110121.en_US
dc.identifier.doi10.1016/j.cellsig.2021.110121
dc.identifier.issn0898-6568
dc.identifier.pmid34438017
dc.identifier.scopus2-s2.0-85113761195
dc.identifier.scopusqualityQ2
dc.identifier.startpage110121en_US
dc.identifier.urihttps://www.sciencedirect.com/science/article/pii/S0898656821002102?via%3Dihub
dc.identifier.urihttps://hdl.handle.net/11468/9353
dc.identifier.volume87en_US
dc.identifier.wosWOS:000702705800007
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorKızıl, Murat
dc.language.isoenen_US
dc.publisherElsevier Inc.en_US
dc.relation.ispartofCellular Signalling
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectAutoimmunityen_US
dc.subjectCOVID-19en_US
dc.subjectCYP450en_US
dc.subjectFoxP3en_US
dc.subjectInflammationen_US
dc.subjectNF-κBen_US
dc.subjectRetinoic aciden_US
dc.subjectRetinoid signalingen_US
dc.subjectRetinolen_US
dc.subjectRIG-Ien_US
dc.subjectRORγten_US
dc.subjectTh17en_US
dc.subjectTregen_US
dc.subjectType-I IFNen_US
dc.subjectVitamin Aen_US
dc.subjectVitamin Den_US
dc.titleA novel hypothesis for COVID-19 pathogenesis: Retinol depletion and retinoid signaling disorderen_US
dc.titleA novel hypothesis for COVID-19 pathogenesis: Retinol depletion and retinoid signaling disorder
dc.typeArticleen_US

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