Evidence map›Paper›PMID 34290349›Full record

ArticleCommunications biology2021

Dynamin-related protein 1 deficiency accelerates lipopolysaccharide-induced acute liver injury and inflammation in mice.

Lixiang Wang, Xin Li, Yuki Hanada, Nao Hasuzawa, Yoshinori Moriyama, Masatoshi Nomura, Ken Yamamoto

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 25 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

7 authors at 4 institutions in 2 countries.

Lixiang WangDepartment of Medical Biochemistry, Kurume University School of Medicine, Kurume, Japan. ourika0211@med.kurume-u.ac.jp.ORCID 0000-0003-2087-4787
Xin LiDepartment of Molecular Pathobiology, New York University College of Dentistry, New York, NY, USA.
Yuki HanadaDepartment of Medicine and Bioregulatory Science, Graduate School of Medical Science, Kyushu University, Higashi-ku, Fukuoka, Japan.ORCID 0000-0003-4610-9338
Nao HasuzawaDivision of Endocrinology and Metabolism, Department of Internal Medicine, Kurume University School of Medicine, Kurume, Japan.
Yoshinori MoriyamaDivision of Endocrinology and Metabolism, Department of Internal Medicine, Kurume University School of Medicine, Kurume, Japan.
Masatoshi NomuraDepartment of Medicine and Bioregulatory Science, Graduate School of Medical Science, Kyushu University, Higashi-ku, Fukuoka, Japan. nomura@med.kurume-u.ac.jp.ORCID 0000-0002-0725-3161
Ken YamamotoDepartment of Medical Biochemistry, Kurume University School of Medicine, Kurume, Japan.ORCID 0000-0002-1531-9685
Kurume University · JPKyushu University · JPKurume University Medical Center · JPNew York University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial fusion and fission, which are strongly related to normal mitochondrial function, are referred to as mitochondrial dynamics. Mitochondrial fusion defects in the liver cause a non-alcoholic steatohepatitis-like phenotype and liver cancer. However, whether mitochondrial fission defect directly impair liver function and stimulate liver disease progression, too, is unclear. Dynamin-related protein 1 (DRP1) is a key factor controlling mitochondrial fission. We hypothesized that DRP1 defects are a causal factor directly involved in liver disease development and stimulate liver disease progression. Drp1 defects directly promoted endoplasmic reticulum (ER) stress, hepatocyte death, and subsequently induced infiltration of inflammatory macrophages. Drp1 deletion increased the expression of numerous genes involved in the immune response and DNA damage in Drp1LiKO mouse primary hepatocytes. We administered lipopolysaccharide (LPS) to liver-specific Drp1-knockout (Drp1LiKO) mice and observed an increased inflammatory cytokine expression in the liver and serum caused by exaggerated ER stress and enhanced inflammasome activation. This study indicates that Drp1 defect-induced mitochondrial dynamics dysfunction directly regulates the fate and function of hepatocytes and enhances LPS-induced acute liver injury in vivo.

Indexed as

AnimalsChemical and Drug Induced Liver InjuryDynaminsInflammationLipopolysaccharidesMaleMiceMice, Inbred C57BLDnm1l protein, mouseDynaminsLipopolysaccharides

Identifiers

PMID34290349
PMCPMC8295278
OpenAlexW3185950660

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.