Evidence map›Paper›PMID 31250532›Full record

ArticleHepatology research : the official journal of the Japan Society of Hepatology2019

Chitinase 3-like 1 deficiency ameliorates liver fibrosis by promoting hepatic macrophage apoptosis.

Masaaki Higashiyama, Kengo Tomita, Nao Sugihara, Hiroyuki Nakashima, Hirotaka Furuhashi, Makoto Nishikawa, Kenichi Inaba, Akinori Wada, Kazuki Horiuchi, Yoshinori Hanawa and 12 more

Open access · hybridAbstract read
In one paragraph

Article in Hepatology research : the official journal of the Japan Society of Hepatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 17% 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, 1 synthesis or guideline pooled it, 49 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

22 authors at 3 institutions in 1 country.

Masaaki HigashiyamaDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Tokorozawa.
Kengo TomitaDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Tokorozawa.
Nao SugiharaDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Tokorozawa.
Hiroyuki NakashimaDepartments of Immunology and Microbiology, Tokorozawa.
Hirotaka FuruhashiDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Tokorozawa.
Makoto NishikawaDepartments of Surgery, National Defense Medical College, Tokorozawa.
Kenichi InabaDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Tokorozawa.
Akinori WadaDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Tokorozawa.
Kazuki HoriuchiDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Tokorozawa.
Yoshinori HanawaDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Tokorozawa.
Naoki ShibuyaDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Tokorozawa.
Chie KuriharaDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Tokorozawa.
Yoshikiyo OkadaDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Tokorozawa.
Shin NishiiDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Tokorozawa.
Akinori MizoguchiDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Tokorozawa.
Hideaki HozumiDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Tokorozawa.
Chikako WatanabeDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Tokorozawa.
Shunsuke KomotoDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Tokorozawa.
Junji YamamotoDepartments of Surgery, National Defense Medical College, Tokorozawa.
Shuhji SekiDepartments of Immunology and Microbiology, Tokorozawa.
Soichiro MiuraDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Tokorozawa.
Ryota HokariDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Tokorozawa.
National Defense Medical College Hospital · JPNational Defense Medical College · JPInternational University of Health and Welfare · JP

Funding

Ministry of Education, Culture, Sports, Science, and Technology of Japan
6 · The paper itself

Abstract

aimChitinase 3-like 1 (CHI3L1), an 18-glycosyl hydrolase-related molecule, is a member of the enzymatically inactive chitinase-like protein family. Serum levels of CHI3L1 are strongly correlated with hepatic fibrosis progression during many liver diseases. Therefore, this protein could be involved in the development of hepatic fibrosis pathology; however, its role has not been elucidated. We aimed to elucidate its role in the pathophysiology of liver fibrosis.

methodsChitinase 3-like 1-deficient (Chi3l1

resultsIn human and mouse fibrotic livers, CHI3L1 expression was mainly localized to hepatic macrophages, and the intrahepatic accumulation of CHI3L1

conclusionsChitinase 3-like 1 exacerbates liver fibrosis progression by suppressing apoptosis in hepatic macrophages. Therefore, this might be a potential therapeutic target for the treatment of liver fibrosis.

Indexed as

Aktchitinase 3-like 1Fasliver fibrosismacrophage

Identifiers

PMID31250532
PMCPMC6916176
OpenAlexW2955432337

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.