Evidence map›Paper›PMID 31547152›Full record

ArticleCancers2019

Hepatic Stress Response in HCV Infection Promotes STAT3-Mediated Inhibition of HNF4A-

Yucel Aydin, Ramazan Kurt, Kyoungsub Song, Dong Lin, Hanadi Osman, Brady Youngquist, John W Scott, Nathan J Shores, Paul Thevenot, Ari Cohen and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.8field-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

22 citing papers in PubMed, 40 citations in OpenAlex.

  1. Hepatocyte nuclear factor 4-Alpha: a key regulator in liver carcinogenesis.Cellular oncology (Dordrecht, Netherlands) · 2025
    Review
  2. Hepatocyte Nuclear Factor 4 Alpha: A Key Regulator of Liver Disease Pathology and Haemostatic Disorders.Liver international : official journal of the International Association for the Study of the Liver · 2025
    Review
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  5. The therapeutic potential of exosomes in lung cancer.Cellular oncology (Dordrecht, Netherlands) · 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

11 authors at 2 institutions in 1 country.

Yucel AydinDepartment of Pathology and Laboratory Medicine, Tulane University Health Sciences Center, New Orleans, LA 70112, USA. yaydin@tulane.edu.ORCID 0000-0001-6727-6296
Ramazan KurtSection of Gastroenterology and Hepatology, Tulane University Health Sciences Center, New Orleans, LA 70112, USA. rkurt@tulane.edu.
Kyoungsub SongDepartment of Pathology and Laboratory Medicine, Tulane University Health Sciences Center, New Orleans, LA 70112, USA. ksong@tulane.edu.
Dong LinDepartment of Pathology and Laboratory Medicine, Tulane University Health Sciences Center, New Orleans, LA 70112, USA. dlin6@tulane.edu.
Hanadi OsmanDepartment of Pathology and Laboratory Medicine, Tulane University Health Sciences Center, New Orleans, LA 70112, USA. hosman1@tulane.edu.
Brady YoungquistDepartment of Pathology and Laboratory Medicine, Tulane University Health Sciences Center, New Orleans, LA 70112, USA. byoungquist@tulane.edu.
John W ScottDepartment of Pathology and Laboratory Medicine, Tulane University Health Sciences Center, New Orleans, LA 70112, USA. jscottmd@tulane.edu.
Nathan J ShoresSection of Gastroenterology and Hepatology, Tulane University Health Sciences Center, New Orleans, LA 70112, USA. shoresnj@gmail.com.
Paul ThevenotLiver Transplant Surgery Section, Ochsner Medical Center, New Orleans, LA 70121, USA. paul.thevenot@oschner.org.
Ari CohenLiver Transplant Surgery Section, Ochsner Medical Center, New Orleans, LA 70121, USA. acohen@oschner.org.
Srikanta DashDepartment of Pathology and Laboratory Medicine, Tulane University Health Sciences Center, New Orleans, LA 70112, USA. sdash@tulane.edu.
Tulane University · USOchsner Medical Center · US

Funding

Tracking & Evaluation CoreU54GM104940 · NIGMS · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI Peter Todd Katzmarzyk · 2012 to 2026
$69.1M
NIGMS NIH HHS U54 GM104940NIH HHS 1P20GM11288-01NIH HHS AI103106NIH HHS CA089121VA Merit Review Grant 1I0OBX004516-01A1
6 · The paper itself

Abstract

Hepatitis C virus (HCV) infection compromises the natural defense mechanisms of the liver leading to a progressive end stage disease such as cirrhosis and hepatocellular carcinoma (HCC). The hepatic stress response generated due to viral replication in the endoplasmic reticulum (ER) undergoes a stepwise transition from adaptive to pro-survival signaling to improve host cell survival and liver disease progression. The minute details of hepatic pro-survival unfolded protein response (UPR) signaling that contribute to HCC development in cirrhosis are unknown. This study shows that the UPR sensor, the protein kinase RNA-like ER kinase (PERK), mediates the pro-survival signaling through nuclear factor erythroid 2-related factor 2 (NRF2)-mediated signal transducer and activator of transcription 3 (STAT3) activation in a persistent HCV infection model of Huh-7.5 liver cells. The NRF2-mediated STAT3 activation in persistently infected HCV cell culture model resulted in the decreased expression of hepatocyte nuclear factor 4 alpha (HNF4A), a major liver-specific transcription factor. The stress-induced inhibition of HNF4A expression resulted in a significant reduction of liver-specific

Indexed as

cirrhosisendoplasmic reticulum (ER) stresshepatitis C virus (HCV)hepatocellular carcinoma (HCC)hepatocyte nuclear factor 4 alpha (HNF4A)microRNA-122 (miR-122)nuclear factor erythroid 2-related factor 2 (NRF2)oxidative stress (OS)signal transducer and activator of transcription 3 (STAT3)unfolded protein response (UPR)

Identifiers

PMID31547152
PMCPMC6827087
OpenAlexW2974036464

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.