Evidence map›Paper›PMID 34626074›Full record

ArticleJournal of cellular and molecular medicine2021

DHFR silence alleviated the development of liver fibrosis by affecting the crosstalk between hepatic stellate cells and macrophages.

Yu Peng, Zedong Li, Sheng Chen, Jun Zhou

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. 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
1.5field-weighted citation impact, top 16% 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, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Role of Exosomal Modulation of Macrophages in Liver Fibrosis.Journal of clinical and translational hepatology · 2024
    Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
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

4 authors at 1 institution in 1 country.

Yu PengDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, China.
Zedong LiDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, China.
Sheng ChenDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, China.
Jun ZhouDepartment of Emergency Medicine, The Second Xiangya Hospital, Central South University, Changsha, China.ORCID 0000-0001-8372-6576
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver fibrogenesis is a dynamic cellular and tissue process which has the potential to progress into cirrhosis of even liver cancer and liver failure. The activation of hepatic stellate cells (HSCs) is the central event underlying liver fibrosis. Besides, hepatic macrophages have been proposed as potential targets in combatting fibrosis. As for the relationship between HSCs and hepatic macrophages in liver fibrosis, it is generally considered that macrophages promoted liver fibrosis via activating HSCs. However, whether activated HSCs could in turn affect macrophage polarization has rarely been studied. In this study, mRNAs with significant differences were explored using exosomal RNA-sequencing of activated Lx-2 cells and normal RNA-sequencing of DHFR loss-of-function Lx-2 cell models. Cell functional experiments in both Lx-2 cells and macrophages animal model experiments were performed. The results basically confirmed exosomes secreted from activated HSCs could promote M1 polarization of macrophages further. Exosome harbouring DHFR played an important role in this process. DHFR silence in HSCs could decrease Lx-2 activation and M1 polarization of M0 macrophages and then alleviate the development of liver fibrosis both in vitro and vivo. Our work brought a new insight that exosomal DHFR derived from HSCs had a crucial role in crosstalk between HSCs activation and macrophage polarization, which may be a potential therapeutic target in liver fibrosis.

Indexed as

Gene SilencingAnimalsBiomarkersCell CommunicationCell LineDisease Models, AnimalDisease SusceptibilityExosomesGene Expression ProfilingGene Knockdown TechniquesHepatic Stellate CellsHumansLiver CirrhosisMacrophage ActivationMacrophagesMaleBiomarkersINPP5D protein, humanPhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesTetrahydrofolate Dehydrogenaseexosomeshepatic stellate cellsliver fibrosismacrophages

Identifiers

PMID34626074
PMCPMC8572769
OpenAlexW3203580718

What OpenQuestion holds

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LicenceCC BY
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.