Evidence map›Paper›PMID 28285394›Full record

ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2017

HCV-induced regulatory alterations of IL-1β, IL-6, TNF-α, and IFN-ϒ operative, leading liver en-route to non-alcoholic steatohepatitis.

Rabia Nawaz, Sadia Zahid, Muhammad Idrees, Shazia Rafique, Muhammad Shahid, Ammara Ahad, Iram Amin, Iqra Almas, Samia Afzal

Abstract readReview
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In one paragraph

Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

15 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

9 authors.

Rabia NawazNational Center of Excellence in Molecular Biology, University of the Punjab, Lahore, 54590, Pakistan.
Sadia ZahidNational Center of Excellence in Molecular Biology, University of the Punjab, Lahore, 54590, Pakistan.
Muhammad IdreesHazara University, Khyber Pakhtunkhawa, Dhodial, Pakistan.
Shazia RafiqueNational Center of Excellence in Molecular Biology, University of the Punjab, Lahore, 54590, Pakistan.
Muhammad ShahidNational Center of Excellence in Molecular Biology, University of the Punjab, Lahore, 54590, Pakistan.
Ammara AhadNational Center of Excellence in Molecular Biology, University of the Punjab, Lahore, 54590, Pakistan.
Iram AminNational Center of Excellence in Molecular Biology, University of the Punjab, Lahore, 54590, Pakistan.
Iqra AlmasNational Center of Excellence in Molecular Biology, University of the Punjab, Lahore, 54590, Pakistan.
Samia AfzalNational Center of Excellence in Molecular Biology, University of the Punjab, Lahore, 54590, Pakistan. samiaraza@live.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Over the course of time, Hepatitis C has become a universal health menace. Its deleterious effects on human liver encompass a lot of physiological, genetic as well as epigenetic alterations. Fatty liver (Hepatic steatosis) is an inflammation having multifactorial ancestries; one of them is HCV (steatohepatitis). HCV boosts several cellular pathways involving up-regulation of a number of cytokines. Current study reviews the regulation of some selective key cytokines during HCV infection, to help generate an improved understanding of their role. These cytokines, IL-1β, IL-6, TNF-α, and IFN-ϒ, are inflammatory markers of the body. These particular markers along with others help hepatocytes against viral infestation. However, recently, their association has been found in degradation of liver on the trail heading to non-alcoholic steatohepatitis (NASH). Consequently, the disturbance in their equilibrium has been repeatedly reported during HCV infection. Quite a number of findings are affirming their up-regulation. Although these cell markers are stimulated by hepatocytes as their standard protection mechanism, but modern studies have testified the paradoxical nature of this defense line. Nevertheless, direct molecular or epigenetic research is needed to question the actual molecular progressions and directions commanding liver to steatosis, cirrhosis, or eventually HCC (Hepatocellular Carcinoma).

Indexed as

AnimalsCytokinesHepacivirusHepatitis CHumansLiverNon-alcoholic Fatty Liver DiseaseCytokinesHepatitis C virus (HCV)Interferon (IFN)Interleukins (IL)Non-alcoholic steatohepatitis (NASH)Tumor necrosis factor (TNF)

Identifiers

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.