Evidence map›Paper›PMID 33436955›Full record

ArticleScientific reports2021

LECT2 as a hepatokine links liver steatosis to inflammation via activating tissue macrophages in NASH.

Noboru Takata, Kiyo-Aki Ishii, Hiroaki Takayama, Mayumi Nagashimada, Kyoko Kamoshita, Takeo Tanaka, Akihiro Kikuchi, Yumie Takeshita, Yukako Matsumoto, Tsuguhito Ota and 6 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
7.2field-weighted citation impact, top 2% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. A LECT2-elutingMaterials today. Bio · 2026
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  11. Elevated LECT2 and PEDF in Pediatric MAFLD: Diagnostic Performance and Metabolic Correlations.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025
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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

16 authors at 2 institutions in 1 country.

Noboru TakataDepartment of Endocrinology and Metabolism, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, 920-8640, Japan.
Kiyo-Aki IshiiDepartment of Integrative Medicine for Longevity, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, 920-8640, Japan.
Hiroaki TakayamaDepartment of Endocrinology and Metabolism, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, 920-8640, Japan.
Mayumi NagashimadaTechnology Department of Clinical Laboratory Science, Kanazawa University Graduate School of Medical Science and Technology, Kanazawa, Ishikawa, 920-0942, Japan.
Kyoko KamoshitaDepartment of Endocrinology and Metabolism, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, 920-8640, Japan.
Takeo TanakaDepartment of Endocrinology and Metabolism, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, 920-8640, Japan.
Akihiro KikuchiDepartment of Endocrinology and Metabolism, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, 920-8640, Japan.
Yumie TakeshitaDepartment of Endocrinology and Metabolism, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, 920-8640, Japan.
Yukako MatsumotoDepartment of Endocrinology and Metabolism, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, 920-8640, Japan.
Tsuguhito OtaDepartment of Endocrinology and Metabolism, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, 920-8640, Japan.
Yasuhiko YamamotoDepartment of Biochemistry and Molecular Vascular Biology, Kanazawa University Graduate School of Medical Science, Kanazawa, Ishikawa, 920-8640, Japan.
Satoshi YamagoeDepartment of Chemotherapy and Mycoses, National Institute of Infectious Diseases, Shinjuku-ku, Tokyo, 162-8640, Japan.
Akihiro SekiDepartment of Gastroenterology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, 920-8640, Japan.
Yoshio SakaiDepartment of Gastroenterology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, 920-8640, Japan.
Shuichi KanekoDepartment of Gastroenterology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, 920-8640, Japan.
Toshinari TakamuraDepartment of Endocrinology and Metabolism, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, 920-8640, Japan. ttakamura@med.kanazawa-u.ac.jp.ORCID 0000-0002-4393-3244
Kanazawa University · JPNational Institute of Infectious Diseases · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It remains unclear how hepatic steatosis links to inflammation. Leukocyte cell-derived chemotaxin 2 (LECT2) is a hepatokine that senses fat in the liver and is upregulated prior to weight gain. The aim of this study was to investigate the significance of LECT2 in the development of nonalcoholic steatohepatitis (NASH). In human liver biopsy samples, elevated LECT2 mRNA levels were positively correlated with body mass index (BMI) and increased in patients who have steatosis and inflammation in the liver. LECT2 mRNA levels were also positively correlated with the mRNA levels of the inflammatory genes CCR2 and TLR4. In C57BL/6J mice fed with a high-fat diet, mRNA levels of the inflammatory cytokines Tnfa and Nos2 were significantly lower in Lect2 KO mice. In flow cytometry analyses, the number of M1-like macrophages and M1/M2 ratio were significantly lower in Lect2 KO mice than in WT mice. In KUP5, mouse kupffer cell line, LECT2 selectively enhanced the LPS-induced phosphorylation of JNK, but not that of ERK and p38. Consistently, LECT2 enhanced the LPS-induced phosphorylation of MKK4 and TAB2, upstream activators of JNK. Hepatic expression of LECT2 is upregulated in association with the inflammatory signature in human liver tissues. The elevation of LECT2 shifts liver residual macrophage to the M1-like phenotype, and contributes to the development of liver inflammation. These findings shed light on the hepatokine LECT2 as a potential therapeutic target that can dissociate liver steatosis from inflammation.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCell LineDiet, High-FatGene ExpressionInflammationIntercellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesKupffer CellsLiverMacrophage ActivationMiceMice, Inbred C57BLMolecular Targeted TherapyNon-alcoholic Fatty Liver DiseasePhosphorylationAdaptor Proteins, Signal TransducingIntercellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesLect2 protein, mouseRNA, MessengerTab2 protein, mouse

Identifiers

PMID33436955
PMCPMC7804418
OpenAlexW3120193952

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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.