Evidence map›Paper›PMID 25253946›Full record

ReviewWorld journal of gastroenterology2014

Potential mechanisms of hepatitis B virus induced liver injury.

Mohd Suhail, Hany Abdel-Hafiz, Ashraf Ali, Kaneez Fatima, Ghazi A Damanhouri, Esam Azhar, Adeel Ga Chaudhary, Ishtiaq Qadri

Open access · bronzeAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

40 citing papers in PubMed, 70 citations in OpenAlex.

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  18. Contribution of Aflatoxin BInternational journal of general medicine · 2023
    Article
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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.

Mohd SuhailMohd Suhail, Ashraf Ali, Ghazi A Damanhouri, Adeel GA Chaudhary, Ishtiaq Qadri, King Fahd Medical Research Center, King Abdul Aziz University, Jeddah 21589, Saudi Arabia.
Hany Abdel-HafizMohd Suhail, Ashraf Ali, Ghazi A Damanhouri, Adeel GA Chaudhary, Ishtiaq Qadri, King Fahd Medical Research Center, King Abdul Aziz University, Jeddah 21589, Saudi Arabia.
Ashraf AliMohd Suhail, Ashraf Ali, Ghazi A Damanhouri, Adeel GA Chaudhary, Ishtiaq Qadri, King Fahd Medical Research Center, King Abdul Aziz University, Jeddah 21589, Saudi Arabia.
Kaneez FatimaMohd Suhail, Ashraf Ali, Ghazi A Damanhouri, Adeel GA Chaudhary, Ishtiaq Qadri, King Fahd Medical Research Center, King Abdul Aziz University, Jeddah 21589, Saudi Arabia.
Ghazi A DamanhouriMohd Suhail, Ashraf Ali, Ghazi A Damanhouri, Adeel GA Chaudhary, Ishtiaq Qadri, King Fahd Medical Research Center, King Abdul Aziz University, Jeddah 21589, Saudi Arabia.
Esam AzharMohd Suhail, Ashraf Ali, Ghazi A Damanhouri, Adeel GA Chaudhary, Ishtiaq Qadri, King Fahd Medical Research Center, King Abdul Aziz University, Jeddah 21589, Saudi Arabia.
Adeel Ga ChaudharyMohd Suhail, Ashraf Ali, Ghazi A Damanhouri, Adeel GA Chaudhary, Ishtiaq Qadri, King Fahd Medical Research Center, King Abdul Aziz University, Jeddah 21589, Saudi Arabia.
Ishtiaq QadriMohd Suhail, Ashraf Ali, Ghazi A Damanhouri, Adeel GA Chaudhary, Ishtiaq Qadri, King Fahd Medical Research Center, King Abdul Aziz University, Jeddah 21589, Saudi Arabia.
King Abdul Aziz University Hospital · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic active hepatitis (CAH) is acknowledged as an imperative risk factor for the development of liver injury and hepatocellular carcinoma. The histological end points of CAH are chronic inflammation, fibrosis and cirrhosis which are coupled with increased DNA synthesis in cirrhotic vs healthy normal livers. The potential mechanism involved in CAH includes a combination of processes leading to liver cell necrosis, inflammation and cytokine production and liver scaring (fibrosis). The severity of liver damage is regulated by Hepatitis B virus genotypes and viral components. The viral and cellular factors that contribute to liver injury are discussed in this article. Liver injury caused by the viral infection affects many cellular processes such as cell signaling, apoptosis, transcription, DNA repair which in turn induce radical effects on cell survival, growth, transformation and maintenance. The consequence of such perturbations is resulted in the alteration of bile secretion, gluconeogenesis, glycolysis, detoxification and metabolism of carbohydrates, proteins, fat and balance of nutrients. The identification and elucidation of the molecular pathways perturbed by the viral proteins are important in order to design effective strategy to minimize and/or restore the hepatocytes injury.

Indexed as

AnimalsBiomarkers, TumorCarcinoma, HepatocellularGenotypeHepatitis B, ChronicHepatitis B virusHost-Pathogen InteractionsHumansInflammation MediatorsLiverLiver CirrhosisLiver NeoplasmsSignal TransductionViral ProteinsBiomarkers, TumorInflammation MediatorsViral ProteinsGround squirrel hepatitis virusHepatitis B virusHepatitis B virus genotypeHepatocellular carcinomaInterferon regulatory factor 7Interleukin-1 receptor-associated kinase 4Peripheral blood mononuclear cellsTNF receptor-associated factor 3Woodchuck hepatitis virus

Identifiers

PMID25253946
PMCPMC4168079
OpenAlexW1998915515

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.