Evidence map›Paper›PMID 28603092›Full record

ReviewHepatobiliary & pancreatic diseases international : HBPD INT2017

Crosstalk of liver immune cells and cell death mechanisms in different murine models of liver injury and its clinical relevance.

Hilal Ahmad Khan, Muhammad Zishan Ahmad, Junaid Ali Khan, Muhammad Imran Arshad

Open access · greenAbstract readReview
In one paragraph

Review in Hepatobiliary & pancreatic diseases international : HBPD INT, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 81 citations in OpenAlex.

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  10. International journal of molecular sciences · 2023
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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

4 authors at 2 institutions in 1 country.

Hilal Ahmad Khan
Muhammad Zishan Ahmad
Junaid Ali Khan
Muhammad Imran ArshadInstitute of Microbiology, University of Agriculture, Faisalabad 38040, Pakistan. drimranarshad@yahoo.com.
University of Agriculture Faisalabad · PKUniversity of Faisalabad · PK

Funding

Higher Education Commission (HEC) at University of Agriculture, Faisalabad, Pakistan 20-4613/NRPU/R&D/HEC/14/45
6 · The paper itself

Abstract

backgroundLiver inflammation or hepatitis is a result of pluripotent interactions of cell death molecules, cytokines, chemokines and the resident immune cells collectively called as microenvironment. The interplay of these inflammatory mediators and switching of immune responses during hepatotoxic, viral, drug-induced and immune cell-mediated hepatitis decide the fate of liver pathology. The present review aimed to describe the mechanisms of liver injury, its relevance to human liver pathology and insights for the future therapeutic interventions. DATA SOURCES: The data of mouse hepatic models and relevant human liver diseases presented in this review are systematically collected from PubMed, ScienceDirect and the Web of Science databases published in English.

resultsThe hepatotoxic liver injury in mice induced by the metabolites of CCl

conclusionsThe mouse animal models of hepatitis provide a parallel approach for the study of human liver pathology. Blocking or stimulating the pathways associated with liver cell death could unveil the novel therapeutic strategies in the management of liver diseases.

Indexed as

Cell CommunicationAnimalsApoptosisChemical and Drug Induced Liver InjuryCytokinesDisease Models, AnimalFas Ligand ProteinHepatitis, Viral, AnimalHost-Pathogen InteractionsHumansInflammation MediatorsLiverMiceNecrosisOxidative StressReactive Oxygen SpeciesCytokinesFas Ligand ProteinFasl protein, mouseInflammation MediatorsReactive Oxygen Species

Identifiers

PMID28603092
PMCPMC7172563
OpenAlexW2610536898

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.