Evidence map›Paper›PMID 30753992›Full record

ArticleMolecular therapy. Nucleic acids2019

Exosomal Transmission of MicroRNA from HCV Replicating Cells Stimulates Transdifferentiation in Hepatic Stellate Cells.

Ji Hyun Kim, Chang Ho Lee, Seong-Wook Lee

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 2 pooled it
4.5field-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

67 citing papers in PubMed, 2 syntheses or guidelines pooled it, 83 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. HBV/HCV coinfection and anti-tuberculosis drug-induced liver injury: from risk assessment and exploration of mechanisms to preventive considerations.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026
    Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Extracellular Vesicles inInternational journal of molecular sciences · 2024
    Review

7 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Ji Hyun KimDepartment of Integrated Life Sciences, Research Institute of Advanced Omics, Dankook University, 152, Jukjeon-ro, Suji-gu, Yongin 16890, Republic of Korea; Department of Molecular Biology, Dankook University, 119, Dandae-ro, Dongnam-gu, Cheonan 31116, Republic of Korea.
Chang Ho LeeDepartment of Integrated Life Sciences, Research Institute of Advanced Omics, Dankook University, 152, Jukjeon-ro, Suji-gu, Yongin 16890, Republic of Korea.
Seong-Wook LeeDepartment of Integrated Life Sciences, Research Institute of Advanced Omics, Dankook University, 152, Jukjeon-ro, Suji-gu, Yongin 16890, Republic of Korea. Electronic address: swl0208@dankook.ac.kr.
Dankook University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mechanism by which hepatitis C virus (HCV) causes fibrosis and other chronic liver diseases remains poorly understood. Previously, we observed that HCV infection induces microRNA-192 (miR-192) expression, which in turn upregulates transforming growth factor β1 (TGF-β1) in hepatocytes. In this study, we aimed to determine the roles and mechanisms of HCV-induced miR-192 expression during chronic liver injury and fibrosis and to identify potential target of the liver disease. Noticeably, miR-192 is secreted and transmitted through exosomes from HCV-replicating hepatocytes into hepatic stellate cells (HSCs). Exosomal transferred miR-192 upregulated fibrogenic markers in HSCs through TGF-β1 upregulation, resulting in the activation and transdifferentiation of HSCs into myofibroblasts. Anti-miR-192 treatment of HCV-replicating hepatocytes efficiently reduced miR-192 levels in exosomes, downregulated miR-192 and fibrogenic marker levels in HSCs, and impeded transdifferentiation of the cells. In contrast, miR-192 mimic RNA treatment significantly increased miR-192 levels in exosomes from naive hepatocytes, increased miR-192 and fibrogenic marker expression in HSCs, and induced transdifferentiation of the cells. Notably, transdifferentiation of exosome-exposed HSCs was reversed following treatment with anti-miR-192 into the HSCs. This study revealed a novel mechanism of HCV-induced liver fibrosis and identified exosomal miR-192 as a major regulator and potential treatment target for HCV-mediated hepatic fibrosis.

Indexed as

exosomefibrogenic markerhepatic stellate cellshepatitis C virushepatocytesliver fibrosismicroRNAmiR-192myofibroblaststransdifferentiation

Identifiers

PMID30753992
PMCPMC6369229
OpenAlexW2909653685

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.