Evidence map›Paper›PMID 34135558›Full record

ArticleWorld journal of gastroenterology2021

Insight into molecular mechanisms underlying hepatic dysfunction in severe COVID-19 patients using systems biology.

Sarah Musa Hammoudeh, Arabella Musa Hammoudeh, Poorna Manasa Bhamidimarri, Bassam Mahboub, Rabih Halwani, Qutayba Hamid, Mohamed Rahmani, Rifat Hamoudi

Open access · hybridAbstract read
In one paragraph

Article in World journal of gastroenterology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Sarah Musa HammoudehSharjah Institute for Medical Research, College of Medicine, University of Sharjah, Sharjah 27272, United Arab Emirates.
Arabella Musa HammoudehCollege of Medicine, University of Sharjah, Sharjah 27272, United Arab Emirates.
Poorna Manasa BhamidimarriSharjah Institute for Medical Research, College of Medicine, University of Sharjah, Sharjah 27272, United Arab Emirates.
Bassam MahboubCollege of Medicine, University of Sharjah, Sharjah 27272, United Arab Emirates.
Rabih HalwaniSharjah Institute for Medical Research, College of Medicine, University of Sharjah, Sharjah 27272, United Arab Emirates.
Qutayba HamidSharjah Institute for Medical Research, College of Medicine, University of Sharjah, Sharjah 27272, United Arab Emirates.
Mohamed RahmaniSharjah Institute for Medical Research, College of Medicine, University of Sharjah, Sharjah 27272, United Arab Emirates.
Rifat HamoudiSharjah Institute for Medical Research, College of Medicine, University of Sharjah, Sharjah 27272, United Arab Emirates. rhamoudi@sharjah.ac.ae.
University of Sharjah · AE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe coronavirus disease 2019 (COVID-19), a pandemic contributing to more than 105 million cases and more than 2.3 million deaths worldwide, was described to be frequently accompanied by extrapulmonary manifestations, including liver dysfunction. Liver dysfunction and elevated liver enzymes were observed in about 53% of COVID-19 patients.

aimTo gain insight into transcriptional abnormalities in liver tissue of severe COVID-19 patients that may result in liver dysfunction.

methodsThe transcriptome of liver autopsy samples from severe COVID-19 patients against those of non-COVID donors was analyzed. Differentially expressed genes were identified from normalized RNA-seq data and analyzed for the enrichment of functional clusters and pathways. The differentially expressed genes were then compared against the genetic signatures of liver diseases including cirrhosis, fibrosis, non-alcoholic fatty liver disease (NAFLD), and hepatitis A/B/C. Gene expression of some differentially expressed genes was assessed in the blood samples of severe COVID-19 patients with liver dysfunction using qRT-PCR.

resultsAnalysis of the differential transcriptome of the liver tissue of severe COVID-19 patients revealed a significant upregulation of transcripts implicated in tissue remodeling including G-coupled protein receptors family genes,

conclusionSevere COVID-19 patients appear to experience significant transcriptional shift that may ensue tissue remodeling, mitochondrial dysfunction and lower hepatic detoxification resulting in the clinically observed liver dysfunction.

Indexed as

COVID-19Non-alcoholic Fatty Liver DiseaseHSP40 Heat-Shock ProteinsHumansLiverSARS-CoV-2Steroid HydroxylasesSystems BiologyTranscriptomeCYP39A1 protein, humanDNAJB1 protein, humanHSP40 Heat-Shock ProteinsSteroid HydroxylasesCOVID-19Drug metabolismHepatic detoxificationHepatic dysfunctionMetabolic pathwaysTissue remodeling

Identifiers

PMID34135558
PMCPMC8173390
OpenAlexW3164612475

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.