Evidence map›Paper›PMID 39604571›Full record

ArticleCell biology and toxicology2024

Human liver progenitor-like cells-derived extracellular vesicles promote liver regeneration during acute liver failure.

Yi Chen, Yuling Wu, Hanyong Sun, Hongdan Zhang, Dan Tang, Tianjie Yuan, Caiyang Chen, Weijian Huang, Xu Zhou, Hongping Wu and 7 more

Abstract read
In one paragraph

Article in Cell biology and toxicology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Animal models accurately representing acute liver failure (Review).International journal of molecular medicine · 2026
    Review
  3. 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

17 authors.

Yi Chen *Department of Anesthesiology / Department of Hepatic Surgery, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200217, China.
Yuling Wu *Department of Anesthesiology / Department of Hepatic Surgery, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200217, China.
Hanyong Sun *Department of Anesthesiology / Department of Hepatic Surgery, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200217, China.
Hongdan ZhangCelliver Biotechnology Co. Ltd., Shanghai, 200120, China.
Dan TangDepartment of Anesthesiology / Department of Hepatic Surgery, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200217, China.
Tianjie YuanDepartment of Anesthesiology / Department of Hepatic Surgery, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200217, China.
Caiyang ChenDepartment of Anesthesiology / Department of Hepatic Surgery, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200217, China.
Weijian HuangDepartment of Anesthesiology / Department of Hepatic Surgery, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200217, China.
Xu ZhouDepartment of Anesthesiology / Department of Hepatic Surgery, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200217, China.
Hongping WuDepartment of Molecular Oncology, Eastern Hepatobiliary Surgery Hospital & National Center of Liver Cancer, Second Military Medical University, Shanghai, 200438, China.
Saihong XuDepartment of Anesthesiology / Department of Hepatic Surgery, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200217, China.
Wenming LiuDepartment of Anesthesiology / Department of Hepatic Surgery, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200217, China.
Yingfu JiaoDepartment of Anesthesiology / Department of Hepatic Surgery, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200217, China.
Liqun YangDepartment of Anesthesiology / Department of Hepatic Surgery, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200217, China.
Qigen LiDepartment of Organ Transplantation, the Second Affiliated Hospital of Nanchang University, Nanchang, 330200, China. qigenli@hotmail.com.
Hexin YanDepartment of Anesthesiology / Department of Hepatic Surgery, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200217, China. hexinyw@163.com.
Weifeng YuDepartment of Anesthesiology / Department of Hepatic Surgery, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200217, China. ywf808@yeah.net.

Funding

National Key Research and Development Program of China 2018YFA0108200National Natural Science Foundation of China 31872823&32030043&82070619Shanghai Engineering Research Center of Peri-operative Organ Support and Function Preservation 20DZ2254200
6 · The paper itself

Abstract

Hepatocyte-derived liver progenitor-like cells (HepLPCs) exhibit a remarkable capacity to support liver function by detoxifying ammonia, promoting native liver regeneration, and suppressing inflammation, which leads to improvements in the recovery and survival of animals with acute liver failure (ALF). However, the mechanism through which HepLPCs promote liver regeneration is unclear. Here, we isolated HepLPC-derived extracellular vesicles (HepLPC-EVs) from conditioned media and performed microRNA sequencing analysis. Our results showed HepLPC-EVs promoted liver regeneration in mice with carbon tetrachloride or acetaminophen induced ALF. Cell cycle progression and proliferation of primary human hepatocytes were promoted after coculture with HepLPC-EVs. Exosomal miRNA sequencing confirmed that HepLPC-EVs were enriched with miR-183-5p, which played an essential role in ameliorating ALF. Mechanistically, HepLPC-derived exosomal miR-183-5p negatively regulated the expression of the target gene FoxO1, activated the Akt/GSK3β/β-catenin signaling pathway, and thereby promoted liver regeneration and restoration of normal liver function. These results indicate that during ALF, HepLPC-Exos mediate liver regeneration mainly through a paracrine exosome-dependent mechanism and these effects accelerate liver regeneration and lead to the restoration of normal liver function.

Indexed as

Extracellular VesiclesHepatocytesLiverLiver Failure, AcuteLiver RegenerationMicroRNAsStem CellsAnimalsCarbon TetrachlorideCell ProliferationExosomesHumansMaleMiceMice, Inbred C57BLSignal TransductionCarbon TetrachlorideMicroRNAsExtracellular vesiclesFoxO1Hepatocyte proliferationLiver progenitor cellsParacrine mechanism

Identifiers

PMID39604571
PMCPMC11602810

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.