Evidence map›Paper›PMID 40637994›Full record

ArticleScience China. Life sciences2025

Liver sinusoidal endothelial cells secret C-X-C motif chemokine ligand 10 to promote the recruitment of invariant NKT cells in acetaminophen-induced liver injury.

Fei Wang, Shuangshuang Zhang, Yan Yao, Penghui Yu, Ke Xue, Xuan Xu, Gaoxiang Li, Hong Zhou

Abstract read
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Article in Science China. Life sciences, 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. Review
  2. Article
  3. Article
  4. Perforin Expression and Natural Killer-Cell Proportion as Biomarkers in Secondary Hemophagocytic Lymphohistiocytosis.Medical science monitor : international medical journal of experimental and clinical research · 2025
    Observational
  5. Review
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.

Fei WangDepartment of Immunology, College of Basic Medical Science, Anhui Medical University, Hefei, 230032, China.
Shuangshuang ZhangDepartment of Immunology, College of Basic Medical Science, Anhui Medical University, Hefei, 230032, China.
Yan YaoDepartment of Immunology, College of Basic Medical Science, Anhui Medical University, Hefei, 230032, China.
Penghui YuDepartment of Cell Biology, College of Life Sciences, Anhui Medical University, Hefei, 230032, China.
Ke XueDepartment of Cell Biology, College of Life Sciences, Anhui Medical University, Hefei, 230032, China.
Xuan XuDepartment of Genetics, College of Life Sciences, Anhui Medical University, Hefei, 230032, China.
Gaoxiang LiDepartment of Immunology, College of Basic Medical Science, Anhui Medical University, Hefei, 230032, China. ligaoxiang@ahmu.edu.cn.
Hong ZhouDepartment of Immunology, College of Basic Medical Science, Anhui Medical University, Hefei, 230032, China. hzhou@ahmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Drug-induced liver injury (DILI) has become a significant public health concern. Liver sinusoidal endothelial cells (LSECs), serving as the primary defense barrier in the liver, play a crucial role in maintaining the sinusoidal microenvironment. However, the adaptive changes occurring in LSECs and the mechanisms that regulate the immune microenvironment during the initial stages of acetaminophen (APAP)-induced liver injury (AILI) remain unclear. Specifically, a significant knowledge gap remains regarding how LSECs interact with immune cells in AILI. In our study, we observed distinct morphological changes in the LSECs during the early stages of AILI. Using single-nuclear RNA sequencing, we identified a disease-specific subpopulation of LSECs, characterized by significant enrichment of biological processes associated with vascular remodeling and cell migration following APAP treatment. Simultaneously, APAP enhanced intercellular communication between LSECs and T/NK cells, with an emphasis on invariant natural killer T (iNKT) cells. Specifically, this LSEC population exhibited significant upregulation of CXCL10, a chemokine that plays a pivotal role in the recruitment of hepatic iNKT and CD4

Indexed as

AcetaminophenChemical and Drug Induced Liver InjuryChemokine CXCL10Endothelial CellsLiverNatural Killer T-CellsAnimalsHumansMaleMiceMice, Inbred C57BLReceptors, CXCR3AcetaminophenChemokine CXCL10Cxcl10 protein, mouseReceptors, CXCR3acetaminophenCXCL10drug-induced liver injuryinvariant natural killer T cellliver sinusoidal endothelial cellsingle-nucleus RNA sequencing

Identifiers

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Registered trials

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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.