Evidence map›Paper›PMID 38745150›Full record

ArticleBMC gastroenterology2024

Hepatic recruitment of myeloid-derived suppressor cells upon liver injury promotes both liver regeneration and fibrosis.

Qiongwen Zhang, Ting Yu, Huaicheng Tan, Huashan Shi

Abstract read
In one paragraph

Article in BMC gastroenterology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
  2. Animal models accurately representing acute liver failure (Review).International journal of molecular medicine · 2026
    Review
  3. Review
  4. Review
  5. Article
  6. 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.

Qiongwen Zhang *Department of Head and Neck Oncology, Cancer Center, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, Sichuan, P.R. China.
Ting Yu *Department of Pathology, West China Hospital, Sichuan University, Chengdu, Sichuan, P.R. China.
Huaicheng TanDepartment of Head and Neck Oncology, Cancer Center, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, Sichuan, P.R. China.
Huashan ShiDepartment of Head and Neck Oncology, Cancer Center, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, Sichuan, P.R. China. shihuashan@scu.edu.cn.

Funding

National Natural Science Foundation of China 81300320Natural Science Foundation of Sichuan Province 2022NSFSC1326
6 · The paper itself

Abstract

backgroundThe liver regeneration is a highly complicated process depending on the close cooperations between the hepatocytes and non-parenchymal cells involving various inflammatory cells. Here, we explored the role of myeloid-derived suppressor cells (MDSCs) in the processes of liver regeneration and liver fibrosis after liver injury.

methodsWe established four liver injury models of mice including CCl

resultsThe intrahepatic infiltrations of MDSCs with surface marker of CD11b

conclusionsThe dramatically and quickly infiltrated CD11b

Indexed as

CD11b AntigenLiver CirrhosisLiver RegenerationMice, Inbred C57BLMyeloid-Derived Suppressor CellsAnimalsBile DuctsCarbon TetrachlorideChemical and Drug Induced Liver InjuryCoculture TechniquesConcanavalin ADisease Models, AnimalHepatic Stellate CellsHepatocytesInterleukin-10LigationCarbon TetrachlorideCD11b AntigenConcanavalin AInterleukin-10LipopolysaccharidesTransforming Growth Factor betaVascular Endothelial Growth Factor ACytokinesLiver fibrosisLiver injuryLiver regenerationMDSCs

Identifiers

PMID38745150
PMCPMC11092103

What OpenQuestion holds

Textmetadata
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.