Evidence map›Paper›PMID 34438017›Full record

ArticleCellular signalling2021

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

Aziz Rodan Sarohan, Murat Kızıl, Ahmet Çağkan İnkaya, Shokhan Mahmud, Muhammad Akram, Osman Cen

Open access · greenAbstract read
In one paragraph

Article in Cellular signalling, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.1field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 48 citations in OpenAlex.

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  12. Review
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  14. Vitamin C Deficiency in Blood Samples of COVID-19 Patients.Antioxidants (Basel, Switzerland) · 2022
    Article
  15. Article
  16. Retinol Depletion in COVID-19.Clinical nutrition open science · 2022
    Article
  17. Observational
  18. Observational
  19. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 5 institutions in 4 countries.

Aziz Rodan SarohanDepartment of Obstetrics and Gynecology, Medicina Plus Medical Center, 75. Yıl Mah., İstiklal Cad. 1305 Sk., No: 16 Sultangazi, İstanbul, Turkey. Electronic address: azizrodan@gmail.com.
Murat KızılDepartment of Chemistry, Faculty of Science, Dicle University. Diyarbakır, Turkey.
Ahmet Çağkan İnkayaDepartment of Infectious Diseases and Clinical Microbiology, Faculty of Medicine, Hacettepe University, Ankara 06230, Turkey.
Shokhan MahmudDepartment of Pharmacognosy, College of Pharmacy, Hawler Medical University, Erbil, Kurdistan Region, Iraq.
Muhammad AkramDepartment of Eastern Medicine Government College, University Faisalabad, Pakistan.
Osman CenDepartment of Microbiology and Immunology, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States of America; Department of Natural Sciences and Engineering, John Wood College, Quincy, IL, United States of America.
Dicle University · TRGovernment College University, Faisalabad · PKHacettepe University · TRHawler Medical University · IQNorthwestern University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The 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.

Indexed as

Central Nervous SystemCOVID-19DEAD Box Protein 58HumansImmune ToleranceInterferon Type IReceptors, ImmunologicSARS-CoV-2Signal TransductionT-Lymphocytes, RegulatoryViral TropismVitamin ADEAD Box Protein 58Interferon Type IReceptors, ImmunologicRIGI protein, humanVitamin AAutoimmunityCOVID-19CYP450FoxP3InflammationNF-κBRetinoic acidRetinoid signalingRetinolRIG-IRORγtTh17TregType-I IFNVitamin AVitamin D

Identifiers

PMID34438017
PMCPMC8380544
OpenAlexW3193733845

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.