Evidence map›Paper›PMID 31409825›Full record

ArticleScientific reports2019

RORα suppresses interleukin-6-mediated hepatic acute phase response.

Ju-Yeon Kim, Yong-Hyun Han, Min-Woo Nam, Hyeon-Ji Kim, Mi-Ock Lee

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Digoxin mitigates diethylnitrosamine-induced acute liver injury in mice via limiting production of inflammatory mediators.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2022
    Article
  8. Article
  9. ROR: Nuclear Receptor for Melatonin or Not?Molecules (Basel, Switzerland) · 2021
    Review
  10. Review
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

5 authors at 1 institution in 2 countries.

Ju-Yeon KimCollege of Pharmacy and Bio-MAX institute, Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, 08826, Republic of Korea.
Yong-Hyun HanCollege of Pharmacy and Bio-MAX institute, Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, 08826, Republic of Korea.
Min-Woo NamCollege of Pharmacy and Bio-MAX institute, Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, 08826, Republic of Korea.
Hyeon-Ji KimCollege of Pharmacy and Bio-MAX institute, Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, 08826, Republic of Korea.
Mi-Ock LeeCollege of Pharmacy and Bio-MAX institute, Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, 08826, Republic of Korea. molee@snu.ac.kr.ORCID http://orcid.org/0000-0002-1578-8211
Seoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute liver failure (ALF) is characterized by loss of liver function in response to sustained augmentation of the acute-phase response (APR) in the liver, which can progress even to death. Although the inflammatory interleukin-6 (IL-6)-axis is a crucial factor that drives the hepatic APR by releasing diverse acute-phase proteins (APPs), therapeutic strategies to block the IL-6-STAT3-mediated APR are not well developed. Here, we show that the nuclear receptor retinoic acid-related orphan receptor α (RORα) limits APR-mediated liver injury by inhibiting the hepatic IL-6-STAT3 signaling pathway. Administration of JC1-40, an RORα activator, diminished diethylnitrosamine-induced acute liver injury and repressed transcriptional expression of APPs such as CXCL1 and LCN2 in mice. IL-6-mediated activation of STAT3 was repressed after RORα activation by either adenoviral infusion of RORα or JC1-40 treatment in primary hepatocytes. Activation of RORα decreased transcriptional expression of IL-6 receptor α, an upstream activator of STAT3, both in vitro and in vivo. This may be one mechanism underlying the RORα-mediated inhibition of STAT3. Taken together, our results suggest that RORα is a regulator of the hepatic IL-6-STAT3 signaling pathway and may be a new therapeutic target for treating APR-associated inflammatory ALF.

Indexed as

Acute-Phase ReactionAdenoviridaeAnimalsChemical and Drug Induced Liver InjuryChemokine CXCL1Deoxyuracil NucleotidesDiethylnitrosamineDisease Models, AnimalGene Expression RegulationHepatocytesHumansHydroxycholesterolsInterleukin-6LiverLiver Failure, AcuteMiceChemokine CXCL1Cxcl1 protein, mouseDeoxyuracil NucleotidesDiethylnitrosamineHydroxycholesterolsInterleukin-6JC 40Nuclear Receptor Subfamily 1, Group F, Member 1Rora protein, mouseSTAT3 Transcription Factor

Identifiers

PMID31409825
PMCPMC6692401
OpenAlexW2968313046

What OpenQuestion holds

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LicenceCC BY
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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.