Evidence map›Paper›PMID 41473257›Full record

ArticleJournal of clinical and translational hepatology2025

PDK4 Regulates Inflammatory Injury in Acute-on-chronic Liver Failure by Phosphorylating STAT1-mediated M1 Polarization of Macrophages.

Shilong Dong, Luyuan Ma, Chuan Shen, Ruolan Gu, Xinyang Li, Ying Xiao, Caiyan Zhao

Abstract read
In one paragraph

Article in Journal of clinical and translational hepatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

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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

2 citing papers in PubMed.

  1. Article
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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

7 authors.

Shilong DongDepartment of Infectious Diseases, Hebei Medical University Third Hospital, Shijiazhuang, Hebei, China.
Luyuan MaDepartment of Infectious Diseases, Hebei Medical University Third Hospital, Shijiazhuang, Hebei, China.
Chuan ShenDepartment of Infectious Diseases, Hebei Medical University Third Hospital, Shijiazhuang, Hebei, China.
Ruolan GuDepartment of Infectious Diseases, Hebei Medical University Third Hospital, Shijiazhuang, Hebei, China.
Xinyang LiDepartment of Infectious Diseases, Hebei Medical University Third Hospital, Shijiazhuang, Hebei, China.
Ying XiaoDepartment of Infectious Diseases, Hebei Medical University Third Hospital, Shijiazhuang, Hebei, China.
Caiyan ZhaoDepartment of Infectious Diseases, Hebei Medical University Third Hospital, Shijiazhuang, Hebei, China.ORCID https://orcid.org/0000-0001-5997-4641

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background and Aims: Acute-on-chronic liver failure (ACLF) is a life-threatening syndrome characterized by systemic inflammation and immune dysregulation, in which macrophages play a key role in organ injury. This study aimed to investigate the role and mechanism of pyruvate dehydrogenase kinase 4 (PDK4) in ACLF to identify therapeutic targets that modulate macrophage function and mitigate ACLF progression. Methods: Single-cell RNA sequencing data from healthy and ACLF liver tissues were analyzed from the Sequence Read Archive database. Transcriptomic data of peripheral blood mononuclear cells from ACLF patients (GSE168048) were also examined. Results: Single-cell analysis revealed a predominance of M1-polarized hepatic macrophages in ACLF with marked upregulation of PDK4. Peripheral blood mononuclear cell transcriptomics showed that higher PDK4 expression correlated with 28-day mortality. Conclusions: PDK4 is a key pro-inflammatory regulator in ACLF by promoting M1 macrophage polarization. Targeting PDK4 may be a promising strategy to attenuate inflammation and improve clinical outcomes in ACLF.

Indexed as

Acute-on-chronic liver failureInflammationM1 polarizationMacrophagePyruvate dehydrogenase kinase 4Signal transducer and activator of transcription 1

Identifiers

PMID41473257
PMCPMC12745191

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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.