Evidence map›Paper›PMID 39910671›Full record

ArticleHuman genomics2025

Liver macrophage-derived exosomal miRNA-342-3p promotes liver fibrosis by inhibiting HPCAL1 in stellate cells.

Wenshuai Li, Lirong Chen, Qi Zhou, Tiansheng Huang, Wanwei Zheng, Feifei Luo, Zhong Guang Luo, Jun Zhang, Jie Liu

Abstract read
In one paragraph

Article in Human genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Myeloid cells in chronic liver inflammation.Cellular & molecular immunology · 2025
    Review
  4. Review
  5. LncRNA HOXA11-AS Promotes Myocardial Injury in Chronic Heart Failure by Sponging miR-342-3p.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis
    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

9 authors.

Wenshuai Li *Department of Digestive Diseases, Huashan Hospital, Fudan University, Shanghai, 200040, China.
Lirong Chen *Department of Digestive Diseases, Huashan Hospital, Fudan University, Shanghai, 200040, China.
Qi Zhou *Department of Digestive Diseases, Huashan Hospital, Fudan University, Shanghai, 200040, China.
Tiansheng HuangDepartment of Digestive Diseases, Shanghai Guanghua Hospital of Integrated Traditional Chinese And Western Medicine, Shanghai, 200040, China.
Wanwei ZhengDepartment of Digestive Diseases, Huashan Hospital, Fudan University, Shanghai, 200040, China.
Feifei LuoDepartment of Digestive Diseases, Huashan Hospital, Fudan University, Shanghai, 200040, China.
Zhong Guang LuoDepartment of Digestive Diseases, Huashan Hospital, Fudan University, Shanghai, 200040, China. luozg8@126.com.
Jun ZhangDepartment of Digestive Diseases, Huashan Hospital, Fudan University, Shanghai, 200040, China. archsteed@163.com.
Jie LiuDepartment of Digestive Diseases, Huashan Hospital, Fudan University, Shanghai, 200040, China. jieliu@fudan.edu.cn.

Funding

National Natural Science Foundation of China Project 82100659Shanghai Sailing Program No.20YF1404200
6 · The paper itself

Abstract

backgroundThe progression of liver fibrosis involves complex interactions between hepatic stellate cells (HSCs) and multiple immune cells in the liver, including macrophages. However, the mechanism of exosomes in the crosstalk between liver macrophages and HSCs remains unclear.

methodExosomes were extracted from primary mouse macrophages and cultured with HSCs, and the differential expression of microRNAs was evaluated using high-throughput sequencing technology. The functions of miR-342-3p in exosomes were verified by qPCR and luciferase reporter gene experiments with HSCs. The function of the target gene Hippocalcin-like protein 1 (HPCAL1) in HSCs was verified by Western blotting, qPCR, cellular immunofluorescence and co-IP in vivo and in vitro.

resultsWe demonstrated that exosomal microRNA-342-3p derived from primary liver macrophages could activate HSCs by inhibiting the expression of HPCAL1 in HSCs. HPCAL1, which is a fibrogenesis suppressor, could inhibit TGF-β signaling in HSCs by regulating the ubiquitination of Smad2 through direct interactions with its EF-hand 4 domain.

conclusionThis study reveals a previously unidentified profibrotic mechanism of crosstalk between macrophages and HSCs in the liver and suggests an attractive novel therapeutic strategy for treating fibroproliferative liver diseases.

Indexed as

Calcium-Binding ProteinsExosomesHepatic Stellate CellsLiver CirrhosisMacrophagesMicroRNAsAnimalsHumansLiverMaleMiceMice, Inbred C57BLSignal TransductionSmad2 ProteinTransforming Growth Factor betaCalcium-Binding ProteinsMicroRNAsSmad2 ProteinTransforming Growth Factor betaExosomeHepatic stellate cellsLiver fibrosisLiver macrophageMiRNA-342-3p

Identifiers

PMID39910671
PMCPMC11800645

What Socratic 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 Socratic graph.