Evidence map›Paper›PMID 34345813›Full record

ArticleJHEP reports : innovation in hepatology2021

Cell fate analysis of zone 3 hepatocytes in liver injury and tumorigenesis.

Shigeyuki Kurosaki, Hayato Nakagawa, Yuki Hayata, Satoshi Kawamura, Yuki Matsushita, Tomoharu Yamada, Koji Uchino, Yoku Hayakawa, Nobumi Suzuki, Masahiro Hata and 7 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in JHEP reports : innovation in hepatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 33 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

17 authors at 3 institutions in 1 country.

Shigeyuki KurosakiDepartment of Gastroenterology, The University of Tokyo, Tokyo, Japan.
Hayato NakagawaDepartment of Gastroenterology, The University of Tokyo, Tokyo, Japan.
Yuki HayataDepartment of Gastroenterology, The University of Tokyo, Tokyo, Japan.
Satoshi KawamuraDepartment of Gastroenterology, The University of Tokyo, Tokyo, Japan.
Yuki MatsushitaDepartment of Gastroenterology, The University of Tokyo, Tokyo, Japan.
Tomoharu YamadaDepartment of Gastroenterology, The University of Tokyo, Tokyo, Japan.
Koji UchinoDepartment of Gastroenterology, The University of Tokyo, Tokyo, Japan.
Yoku HayakawaDepartment of Gastroenterology, The University of Tokyo, Tokyo, Japan.
Nobumi SuzukiDepartment of Gastroenterology, The University of Tokyo, Tokyo, Japan.
Masahiro HataDepartment of Gastroenterology, The University of Tokyo, Tokyo, Japan.
Mayo TsuboiDepartment of Gastroenterology, The University of Tokyo, Tokyo, Japan.
Hiroto KinoshitaDivision of Gastroenterology, Institute for Adult Diseases, Asahi Life Foundation, Tokyo, Japan.
Yasuo TanakaDepartment of Gastroenterology, The University of Tokyo, Tokyo, Japan.
Takuma NakatsukaDepartment of Gastroenterology, The University of Tokyo, Tokyo, Japan.
Yoshihiro HirataDivision of Advanced Genome Medicine, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Keisuke TateishiDepartment of Gastroenterology, The University of Tokyo, Tokyo, Japan.
Kazuhiko KoikeDepartment of Gastroenterology, The University of Tokyo, Tokyo, Japan.
University of Tokyo Hospital · JPInstitute for Adult Diseases Asahi Life Foundation · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsLiver lobules are typically subdivided into 3 metabolic zones: zones 1, 2, and 3. However, the contribution of zonal differences in hepatocytes to liver regeneration, as well as to carcinogenic susceptibility, remains unclear.

methodsWe developed a new method for sustained genetic labelling of zone 3 hepatocytes and performed fate tracing to monitor these cells in multiple mouse liver tumour models.

resultsWe first examined changes in the zonal distribution of the Wnt target gene

conclusionsHepatocytes receiving Wnt/β-catenin signalling from their microenvironment have high neoplastic potential, and Wnt/β-catenin signalling is a potential drug target for the prevention of hepatocellular carcinoma. LAY SUMMARY: Lineage tracing revealed that zone 3 hepatocytes residing in the pericentral niche have high neoplastic potential. Under chronic liver injury, hepatocytes receiving Wnt/β-catenin signalling broadly exist across all hepatic zones and significantly contribute to liver tumorigenesis as well as liver regeneration. Wnt/β-catenin signalling is a potential drug target for the prevention of hepatocellular carcinoma.

Indexed as

CDAHFD, choline-deficient l-amino acid-defined, high-fat dietCPS1, carbamoyl phosphate synthetase 1CYP2E1, cytochrome P450 subfamily 2E1DEN, diethylnitrosamineGS, glutamine synthetaseHAL, histidine ammonia lyaseHCC, hepatocellular carcinomaHepatocellular carcinomaHFD, high-fat dietIF, immunofluorescenceISH, in situ hybridisationLiver regenerationMAFLD, metabolic dysfunction-associated fatty liver diseaseMetabolic dysfunction-associated fatty liver diseaseMetabolic zonationMUP, major urinary proteinND, normal dietPIK3CATg, hepatocyte-specific transgenic mice harbouring mutant PIK3CA variantPP, periportalPV, perivenousRFP, red fluorescent proteinTAM, tamoxifenTUNEL, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labellingWnt/β-catenin signalWT, wild-type

Identifiers

PMID34345813
PMCPMC8319533
OpenAlexW3171779636

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.