Evidence map›Paper›PMID 34410945›Full record

ArticleIn vivo (Athens, Greece)

Recovery of Liver Sinusoidal Endothelial Cells Following Monocrotaline-induced Liver Injury.

Fumisato Otaka, Yoshiya Ito, Takuya Goto, Ken Kojo, Mina Tanabe, Kanako Hosono, Masataka Majima, Wasaburo Koizumi, Hideki Amano

Open access · diamondAbstract read
In one paragraph

Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

9 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
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  6. Obesity and inflammation influence pharmacokinetic profiles of PEG-based nanoparticles.Journal of controlled release : official journal of the Controlled Release Society · 2023
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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.

Fumisato OtakaDepartment of Molecular Pharmacology, Graduate School of Medical Sciences, Kitasato University, Sagamihara, Japan.
Yoshiya ItoDepartment of Molecular Pharmacology, Graduate School of Medical Sciences, Kitasato University, Sagamihara, Japan; yito@kitasto-u.ac.jp.
Takuya GotoDepartment of Molecular Pharmacology, Graduate School of Medical Sciences, Kitasato University, Sagamihara, Japan.
Ken KojoDepartment of Surgery, Kitasato University School of Medicine, Sagamihara, Japan.
Mina TanabeDepartment of Molecular Pharmacology, Graduate School of Medical Sciences, Kitasato University, Sagamihara, Japan.
Kanako HosonoDepartment of Molecular Pharmacology, Graduate School of Medical Sciences, Kitasato University, Sagamihara, Japan.
Masataka MajimaDepartment of Molecular Pharmacology, Graduate School of Medical Sciences, Kitasato University, Sagamihara, Japan.
Wasaburo KoizumiDepartment of Gastroenterology, Kitasato University School of Medicine, Sagamihara, Japan.
Hideki AmanoDepartment of Molecular Pharmacology, Graduate School of Medical Sciences, Kitasato University, Sagamihara, Japan.
Kitasato University · JPKanagawa Institute of Technology · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimAlthough the pathology of sinusoidal obstruction syndrome (SOS) is characterized by damage to liver sinusoidal endothelial cells (LSECs), the processes underlying LSEC repair are incompletely understood. The angiopoietin (Ang)/Tie system contributes to angiogenesis. The present study aimed to examine the processes of LSEC repair and the involvement of the Ang/Tie pathway in LSEC recovery. MATERIALS AND

methodsExperimentally, SOS was induced by intraperitoneal injection of monocrotaline (MCT) to C57/BL6 mice.

resultsLevels of LSEC markers were up-regulated during the repair phase of MCT-induced hepatotoxicity. The damaged LSECs recovered from the injury by expanding LSECs expressing lymphatic vessel endothelial hyaluronan receptor-1 (LYVE-1) in the peri-central area of MCT-injured livers, while LSECs in the same area of uninjured livers lacked LYVE-1 expression. Bone marrow (BM)-derived cells did not incorporate into the restored LSECs. Tie2 expression was related to LSEC recovery in MCT-injured liver tissue.

conclusionThe resident LSECs neighboring uninjured tissue replace damaged LSECs in MCT-injured livers. Tie2 is involved in LSEC recovery from MCT-induced hepatotoxicity.

Indexed as

Chemical and Drug Induced Liver Injury, ChronicMonocrotalineAnimalsEndothelial CellsHepatocytesLiverMiceMonocrotalineangiopoietinLiverLSECmonocrotalinerepairTie2

Identifiers

PMID34410945
PMCPMC8408714
OpenAlexW3193896412

What OpenQuestion holds

Textmetadata
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.