Evidence map›Paper›PMID 38520214›Full record

ArticleJournal of cellular and molecular medicine2024

Hepatocyte-derived exosomes deliver the lncRNA CYTOR to hepatic stellate cells and promote liver fibrosis.

Wenqiang Xu, Wenhui Mo, Dengyu Han, Weiqi Dai, Xiaorong Xu, Jingjing Li, Xuanfu Xu

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

Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Review
  3. 80 years of extracellular vesicles: from discovery to clinical translation.Extracellular vesicles and circulating nucleic acids · 2026
    Review
  4. 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 2 institutions in 1 country.

Wenqiang XuDepartment of Gastroenterology, Shidong Hospital of Shanghai, School of Health Science and Engineering, University of Shanghai for Science and Technology, Shanghai, China.
Wenhui MoDepartment of Gastroenterology, Shidong Hospital of Shanghai, School of Health Science and Engineering, University of Shanghai for Science and Technology, Shanghai, China.
Dengyu HanDepartment of Gastroenterology, Shidong Hospital of Shanghai, School of Health Science and Engineering, University of Shanghai for Science and Technology, Shanghai, China.
Weiqi DaiDepartment of Gastroenterology, Shidong Hospital of Shanghai, School of Health Science and Engineering, University of Shanghai for Science and Technology, Shanghai, China.
Xiaorong XuDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Jingjing LiDepartment of Gastroenterology, Shidong Hospital of Shanghai, School of Health Science and Engineering, University of Shanghai for Science and Technology, Shanghai, China.
Xuanfu XuDepartment of Gastroenterology, Shidong Hospital of Shanghai, School of Health Science and Engineering, University of Shanghai for Science and Technology, Shanghai, China.ORCID 0000-0002-4506-7220
University of Shanghai for Science and Technology · CNTongji University · CN

Funding

National Natural Science Foundation of China 81772591National Natural Science Foundation of China 81970554National Natural Science Foundation of China 82002539National Natural Science Foundation of China 82100638
6 · The paper itself

Abstract

Liver fibrosis is characterized by the activation and transformation of hepatic stellate cells (HSCs) induced by various injury factors. The degree of liver fibrosis can be significantly improved, but persistent injury factors present a significant therapeutic challenge. Hepatocytes are the most important parenchymal cell type in the liver. In this study, we explored the molecular mechanisms by which damaged liver cells activate HSCs through extracellular vesicles. We established a coculture model of LO2 and LX2 and validated its exosomal transmission activity. Subsequently, differentially expressed long noncoding RNAs (lncRNAs) were screened through RNA sequencing and their mechanisms of action as competing endogenous RNAs (ceRNAs) further confirmed using biological methods, such as FISH and luciferase assays. Damaged liver cells induced activation of LX2 and upregulation of liver fibrosis-related markers. Exosomes extracted and identified from the supernatant fraction contained differentially expressed lncRNA cytoskeleton regulator RNA (CYTOR) that competed with microRNA-125 (miR-125) for binding to glial cell line-derived neurotrophic factor (GDNF) in HSCs, in turn, promoting LX2 activation. MiR-125 could target and regulate both CYTOR and GDNF and vice versa, as verified using the luciferase assay. In an in vivo model, damaged liver extracellular vesicles induced the formation of liver fibrosis. Notably, downregulation of CYTOR within extracellular vesicles effectively inhibited liver fibrosis. The lncRNA CYTOR in exosomes of damaged liver cells is upregulated and modulates the expression of downstream GDNF through activity as a ceRNA, providing an effective mechanism for activation of HSCs.

Indexed as

ExosomesMicroRNAsRNA, Long NoncodingGene Expression RegulationGlial Cell Line-Derived Neurotrophic FactorHepatic Stellate CellsHepatocytesHumansLiver CirrhosisLuciferasesGlial Cell Line-Derived Neurotrophic FactorLuciferasesMicroRNAsMIRN125 microRNA, humanRNA, Long NoncodingceRNAexosomeshepatic stellate cellsliver fibrosislncRNA‐CYTOR

Identifiers

PMID38520214
PMCPMC10960169
OpenAlexW4393115536

What OpenQuestion holds

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LicenceCC BY
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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.