Evidence map›Paper›PMID 40268512›Full record

ArticleClinical and translational medicine2025

EEPD1 regulates inflammation and endothelial apoptosis in atherosclerosis through KLF4-EEPD1-ERK axis.

Kaiwen Yu, Xiang Li, Xin Shi, Ruogu Li, Min Zhang

Abstract read
In one paragraph

Article in Clinical and translational medicine, 2025. 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

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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

3 citing papers in PubMed.

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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

5 authors.

Kaiwen YuDepartment of Cardiology, Shanghai Jiao Tong University Affiliated Chest Hospital, Shanghai, China.
Xiang LiDepartment of Cardiology, Shanghai Jiao Tong University Affiliated Chest Hospital, Shanghai, China.
Xin ShiDepartment of Cardiology, Shanghai Jiao Tong University Affiliated Chest Hospital, Shanghai, China.
Ruogu LiDepartment of Cardiology, Shanghai Jiao Tong University Affiliated Chest Hospital, Shanghai, China.
Min ZhangDepartment of Cardiology, Shanghai Jiao Tong University Affiliated Chest Hospital, Shanghai, China.ORCID 0000-0002-4343-7988

Funding

National Natural Science Foundation of China 81900280National Natural Science Foundation of China 82172156National Natural Science Foundation of China 82270298
6 · The paper itself

Abstract

backgroundInflammation and endothelial apoptosis are implicated in the advancement of atherosclerosis. EEPD1 holds a pivotal position in the repair of DNA damage and contributes to the progression of multiple cancers. However, the role of EEPD1 in cardiovascular diseases needs to be explored further, especially in atherosclerosis.

methodsWe constructed EEPD1 and ApoE (apolipoprotein E)-deficient mice to assess how EEPD1 influences endothelial inflammation and apoptosis within atherosclerotic plaques. High-throughput RNA sequencing of human aortic endothelial cell groups treated with siCon+TNFα and siEEPD1+TNFα identified notable disparities in the MAPK pathway between groups. Chromatin immunoprecipitation and luciferase reporter assay confirmed that KLF4 directly regulates EEPD1.

resultsFurther examination of gene expression data revealed elevated EEPD1 concentrations in atherosclerotic plaques of patients, which findings were corroborated in the aortas of ApoE

conclusionsCollectively, this study revealed that EEPD1 deletion can lead to amelioration of atherosclerosis through the KLF4-EEPD1-ERK axis. Hence, targeting EEPD1 could be a promising therapeutic strategy for patients with atherosclerosis.

Indexed as

AtherosclerosisInflammationKruppel-Like Transcription FactorsAnimalsApoptosisEndothelial CellsHumansKruppel-Like Factor 4MaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLKLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription FactorsapoptosisatherosclerosisEEPD1endothelia

Identifiers

PMID40268512
PMCPMC12017893

What Socratic holds

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LicenceCC BY
Read underepoch 390

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 Socratic graph.