Evidence map›Paper›PMID 34676206›Full record

ArticleFrontiers in cell and developmental biology2021

Exosomal miR-500 Derived From Lipopolysaccharide-Treated Macrophage Accelerates Liver Fibrosis by Suppressing MFN2.

Lisha Chen, Yan Huang, Zhixi Duan, Peiqi Huang, Hongbing Yao, Yu Zhou, Qin Ji, Xiangfeng Liu

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

Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.8field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 34 citations in OpenAlex.

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  14. Role of Exosomal Modulation of Macrophages in Liver Fibrosis.Journal of clinical and translational hepatology · 2024
    Review
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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

8 authors at 5 institutions in 1 country.

Lisha ChenCentral Laboratory, Department of Neurosurgery, The Second Xiangya Hospital, Central South University, Changsha, China.
Yan HuangAffiliated Changsha Hospital of Hunan Normal University, The Fourth Hospital of Changsha, Institute of Emergency and Critical Care Medicine of Changsha, Changsha, China.
Zhixi DuanDepartment of Emergency Medicine, Trauma Center, The Second Xiangya Hospital, Central South University, Changsha, China.
Peiqi HuangAffiliated Changsha Hospital of Hunan Normal University, The Fourth Hospital of Changsha, Institute of Emergency and Critical Care Medicine of Changsha, Changsha, China.
Hongbing YaoDepartment of Hepatobiliary and Pancreatic Surgery, The Second Affiliated Hospital, Guilin Medical University, Guilin, China.
Yu ZhouDepartment of Emergency Medicine, Trauma Center, The Second Xiangya Hospital, Central South University, Changsha, China.
Qin JiDepartment of Emergency Medicine, Trauma Center, The Second Xiangya Hospital, Central South University, Changsha, China.
Xiangfeng LiuDepartment of Emergency Medicine, Trauma Center, The Second Xiangya Hospital, Central South University, Changsha, China.
Second Xiangya Hospital of Central South University · CNCentral South University · CNFourth Hospital of Changsha · CNGuilin Medical University · CNHunan Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver fibrosis is an outcome of chronic hepatic injury, which can eventually result in cirrhosis, liver failure, and even liver cancer. The activation of hepatic stellate cell (HSC) is a prominent driver of liver fibrosis. Recently, it has been found that the crosstalk between HSCs and immune cells, including hepatic macrophages, plays an important role in the initiation and development of liver fibrosis. As a vital vehicle of intercellular communication, exosomes transfer specific cargos into HSCs from macrophages. Here, we show that exosomes derived from lipopolysaccharide (LPS)-treated macrophages has higher expression level of miR-500. And overexpression or inhibition of miR-500 in macrophage exosomes could promote or suppress HSC proliferation and activation. Treatment of exosomes with miR-500 overexpression can accelerate liver fibrosis in CCl

Indexed as

exosomehepatic stellate cellliver fibrosismacrophagemiRNA

Identifiers

PMID34676206
PMCPMC8525629
OpenAlexW3203006693

What OpenQuestion holds

Textmetadata
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.