Evidence map›Paper›PMID 29619419›Full record

ArticleHepatology communications2018

Tumor necrosis factor-α-mediated hepatocyte apoptosis stimulates fibrosis in the steatotic liver in mice.

Yosuke Osawa, Ekumi Kojika, Yukiko Hayashi, Masamichi Kimura, Koji Nishikawa, Sachiyo Yoshio, Hiroyoshi Doi, Tatsuya Kanto, Kiminori Kimura

Open access · goldAbstract read
In one paragraph

Article in Hepatology communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 37 citations in OpenAlex.

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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 at 2 institutions in 1 country.

Yosuke OsawaDepartment of Hepatology Tokyo Metropolitan Cancer and Infectious Diseases Center Komagome Hospital Tokyo Japan.
Ekumi KojikaDepartment of Hepatology Tokyo Metropolitan Cancer and Infectious Diseases Center Komagome Hospital Tokyo Japan.
Yukiko HayashiDepartment of Hepatology Tokyo Metropolitan Cancer and Infectious Diseases Center Komagome Hospital Tokyo Japan.
Masamichi KimuraDepartment of Hepatology Tokyo Metropolitan Cancer and Infectious Diseases Center Komagome Hospital Tokyo Japan.
Koji NishikawaDepartment of Hepatology Tokyo Metropolitan Cancer and Infectious Diseases Center Komagome Hospital Tokyo Japan.
Sachiyo YoshioThe Research Center for Hepatitis and Immunology National Center for Global Health and Medicine Chiba Japan.
Hiroyoshi DoiThe Research Center for Hepatitis and Immunology National Center for Global Health and Medicine Chiba Japan.
Tatsuya KantoThe Research Center for Hepatitis and Immunology National Center for Global Health and Medicine Chiba Japan.
Kiminori KimuraDepartment of Hepatology Tokyo Metropolitan Cancer and Infectious Diseases Center Komagome Hospital Tokyo Japan.
Tokyo Metropolitan Komagome Hospital · JPNational Center for Global Health and Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocyte apoptosis has been implicated in the progression of nonalcoholic steatohepatitis. However, it is unclear whether the induction of tumor necrosis factor (TNF)-α-mediated hepatocyte apoptosis in the simple fatty liver triggers liver fibrosis. To address this question, high-fat diet-fed mice were repeatedly administered D-galactosamine, which increases the sensitivity of hepatocytes to TNF-α-mediated apoptosis. In mice treated with a high-fat diet plus D-galactosamine, hepatocyte apoptosis and liver fibrosis were induced, whereas both apoptosis and fibrosis were inhibited in these mice following gut sterilization with antimicrobials or knockout of TNF-α. Furthermore, liver fibrosis was diminished when hepatocyte apoptosis was inhibited by expressing a constitutively active inhibitor of nuclear factor κB kinase subunit β. Thus, hepatocyte apoptosis induced by intestinal dysbiosis or TNF-α up-regulation in the steatotic liver caused fibrosis. Organ fibrosis, including liver fibrosis, involves the interaction of cyclic adenosine monophosphate-response element-binding protein-binding protein (CBP) and β-catenin. Here, hepatocyte-specific CBP-knockout mice showed reduced liver fibrosis accompanied by hepatocyte apoptosis diminution; notably, liver fibrosis was also decreased in mice in which CBP was specifically knocked out in collagen-producing cells because the activation of these cells was now suppressed.

Identifiers

PMID29619419
PMCPMC5880193
OpenAlexW2792352624

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.