Evidence map›Paper›PMID 35500155›Full record

ArticleActa physiologica (Oxford, England)2022

Microbial DNA enrichment promotes liver steatosis and fibrosis in the course of non-alcoholic steatohepatitis.

Zhenlong Luo, Yudong Ji, Dinghong Zhang, Hong Gao, Zhongmou Jin, Meixiang Yang, Wei Ying

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

Article in Acta physiologica (Oxford, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
5.8field-weighted citation impact, top 3% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

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  15. VSIG4Journal of experimental & clinical cancer research : CR · 2025
    Article
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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

7 authors at 4 institutions in 2 countries.

Zhenlong LuoDivision of Endocrinology & Metabolism, Department of Medicine, University of California, San Diego, California, USA.
Yudong JiDivision of Endocrinology & Metabolism, Department of Medicine, University of California, San Diego, California, USA.
Dinghong ZhangDivision of Endocrinology & Metabolism, Department of Medicine, University of California, San Diego, California, USA.
Hong GaoDivision of Endocrinology & Metabolism, Department of Medicine, University of California, San Diego, California, USA.
Zhongmou JinDivision of Biological Sciences, University of California, San Diego, California, USA.
Meixiang YangPediatric Diabetes Research Center, Department of Pediatrics, University of California, San Diego, California, USA.
Wei YingDivision of Endocrinology & Metabolism, Department of Medicine, University of California, San Diego, California, USA.ORCID 0000-0002-4890-7256
University of California San Diego · USJinan University · CNUnion Hospital · CNUniversity of San Diego · US

Funding

Transgenic & Knock-out MouseP30DK063491 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MILES Frome WILKINSON · 2003 to 2026
$40.4M
U of Calif, San Diego Neuroscience Microscopy ImagingP30NS047101 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GLEESON, JOSEPH G, ZHENG, BINHAI · 2003 to 2022
$9.0M
Mechanisms by which hepatocyte extracellular miRNAs mediate peripheral insulin sensitivityR01DK125560 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI YING, WEI · 2021 to 2025
$2.0M
Adipose tissue macrophages secrete exosome-miRs as paracrine/endocrine molecules to directly modulate insulin target cell function in response to obesityR00DK115998 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI YING, WEI · 2020 to 2022
$739k
NIDDK NIH HHS P30 DK063491NIDDK NIH HHS R00 DK115998NIDDK NIH HHS R01 DK125560NINDS NIH HHS P30 NS047101
6 · The paper itself

Abstract

aimLow-grade inflammation is the hallmark of non-alcoholic fatty liver diseases (NAFLD) and non-alcoholic steatohepatitis (NASH). The leakage of microbiota-derived products can contribute to liver inflammation during NAFLD/NASH development. Here, we assessed the roles of gut microbial DNA-containing extracellular vesicles (mEVs) in regulating liver cellular abnormalities in the course of NAFLD/NASH.

methodsWe performed studies with Vsig4

resultsNon-alcoholic fatty liver diseases and non-alcoholic steatohepatitis development was concomitant with a diminished liver Vsig4+ macrophage population and a marked bacterial DNA enrichment in both hepatocytes and HSCs. In the absence of Vsig4+ macrophages, gut mEVs translocation led to microbial DNA accumulation in hepatocytes and HSCs, resulting elevated hepatocyte inflammation and HSC fibrogenic activation. In contrast, in lean WT mice, Vsig4+ macrophages remove gut mEVs from bloodstream through a C3-dependent opsonization mechanism and prevent the infiltration of gut mEVs into hepatic cells. Additionally, Vsig4

conclusionAccumulation of microbial DNAs fuels the development of NAFLD/NASH-associated liver abnormalities.

Indexed as

Non-alcoholic Fatty Liver DiseaseAnimalsDisease Models, AnimalDNA, BacterialFibrosisHepatocytesInflammationLiverMiceMice, Inbred C57BLNucleotidyltransferasesDNA, BacterialNucleotidyltransferasesliver fibrogenic activationliver inflammationmicrobial DNAsmicrobiota-derived extracellular vesiclesVsig4+ macrophages

Identifiers

PMID35500155
PMCPMC9335517
OpenAlexW4225270241

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.