Evidence map›Paper›PMID 28681838›Full record

ArticleNature communications2017

YAP determines the cell fate of injured mouse hepatocytes in vivo.

Norio Miyamura, Shoji Hata, Tohru Itoh, Minoru Tanaka, Miki Nishio, Michiko Itoh, Yoshihiro Ogawa, Shuji Terai, Isao Sakaida, Akira Suzuki and 2 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
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  14. Review
  15. Liver regeneration and ethanol detoxification: A new link in YAP regulation of ALDH1A1 during alcohol-related hepatocyte damage.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  16. Review
  17. Hepatocyte-Specific Deletion of Yes-Associated Protein Improves Recovery From Acetaminophen-Induced Acute Liver Injury.Toxicological sciences : an official journal of the Society of Toxicology · 2021
    Article
  18. Context-dependent roles of YAP/TAZ in stem cell fates and cancer.Cellular and molecular life sciences : CMLS · 2021
    Review
  19. Review
  20. Matrix mechanotransduction mediated by thrombospondin-1/integrin/YAP in the vascular remodeling.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 6 institutions in 1 country.

Norio MiyamuraDepartment of Developmental and Regenerative Biology, Medical Research Institute, Tokyo Medical and Dental University (TMDU), M&D tower 21F, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, Japan.
Shoji HataDepartment of Developmental and Regenerative Biology, Medical Research Institute, Tokyo Medical and Dental University (TMDU), M&D tower 21F, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, Japan.
Tohru ItohLaboratory of Cell Growth and Differentiation, Institute of Molecular and Cellular Biosciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan.ORCID 0000-0002-6579-1638
Minoru TanakaDepartment of Regenerative Medicine, Research Institute, National Center for Global Health and Medicine, 1-21-1 Toyama, Shinjuku-ku, Tokyo 162-8655 Japan.
Miki NishioDivision of Molecular and Cellular Biology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.
Michiko ItohDepartment of Organ Network and Metabolism, Graduate School of Medical and Dental Sciences, TMDU, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, Japan.
Yoshihiro OgawaDepartment of Molecular Endocrinology and Metabolism, Graduate School of Medical and Dental Sciences, TMDU, AMED-CREST, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, Japan.
Shuji TeraiDivision of Gastroenterology and Hepatology, Graduate School of Medical and Dental Sciences, Niigata University, 757, Ichibancho, Asahimachidori, Chuo-ku, Niigata 951-8510, Japan.
Isao SakaidaDepartment of Gastroenterology and Hepatology, Graduate School of Medicine, Yamaguchi University, 1-1-1 Minami-Kogushi, Ube 755-8505, Japan.
Akira SuzukiDivision of Molecular and Cellular Biology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.
Atsushi MiyajimaLaboratory of Cell Growth and Differentiation, Institute of Molecular and Cellular Biosciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan.
Hiroshi NishinaDepartment of Developmental and Regenerative Biology, Medical Research Institute, Tokyo Medical and Dental University (TMDU), M&D tower 21F, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, Japan.
Tokyo Medical and Dental University · JPKobe University · JPThe University of Tokyo · JPNational Center for Global Health and Medicine · JPNiigata University Medical and Dental Hospital · JPYamaguchi University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The presence of senescent, transformed or damaged cells can impair tissue function or lead to tumorigenesis; therefore, organisms have evolved quality control mechanisms to eliminate them. Here, we show that YAP activation induced by inactivation of the Hippo pathway specifically in damaged hepatocytes promotes their selective elimination by using in vivo mosaic analysis in mouse liver. These damaged hepatocytes migrate into the hepatic sinusoids, undergo apoptosis and are engulfed by Kupffer cells. In contrast, YAP activation in undamaged hepatocytes leads to proliferation. Cellular stresses such as ethanol that damage both liver sinusoidal endothelial cells and hepatocytes switch cell fate from proliferation to migration/apoptosis in the presence of activated YAP. This involves the activation of CDC42 and Rac that regulate cell migration. Thus, we suggest that YAP acts as a stress sensor that induces elimination of injured cells to maintain tissue and organ homeostasis.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCarbon Tetrachloridecdc42 GTP-Binding ProteinCell Cycle ProteinsCell MovementChemical and Drug Induced Liver InjuryEthanolFluorescent Antibody TechniqueGene Expression RegulationHepatocytesHippo Signaling PathwayKupffer CellsLiverMaleMiceAdaptor Proteins, Signal TransducingCarbon Tetrachloridecdc42 GTP-Binding ProteinCdc42 protein, mouseCell Cycle ProteinsEthanolMonocrotalinePhosphoproteinsProtein Serine-Threonine Kinasesrac GTP-Binding ProteinsYap1 protein, mouseYAP-Signaling Proteins

Identifiers

PMID28681838
PMCPMC5504293
OpenAlexW2733576316

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.