Evidence map›Paper›PMID 36207452›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2022

ATF3 in atherosclerosis: a controversial transcription factor.

Bingyu Wang, Xi Yang, Xinyi Sun, Jianhui Liu, Yin Fu, Bingyang Liu, Jun Qiu, Jiangfang Lian, Jianqing Zhou

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.4field-weighted citation impact, top 11% of its field
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

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
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  8. Eugenol inhibits preadipocyte differentiation and lipid accumulation via upregulating ATF3.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2025
    Article
  9. Article
  10. Article
  11. Review
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  14. The multifaceted roles of activating transcription factor 3 (ATF3) in inflammatory responses - Potential target to regulate neuroinflammation in acute brain injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
    Review
  15. Review
  16. Article
  17. 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

9 authors at 1 institution in 1 country.

Bingyu WangDepartment of Cardiovascular, Medical College, Ningbo University, Ningbo, China.
Xi YangDepartment of Cardiovascular, Medical College, Ningbo University, Ningbo, China.
Xinyi SunDepartment of Cardiovascular, Medical College, Ningbo University, Ningbo, China.
Jianhui LiuDepartment of Cardiovascular, Lihuili Hospital Affiliated to Ningbo University, Ningbo, China.
Yin FuDepartment of Cardiovascular, Medical College, Ningbo University, Ningbo, China.
Bingyang LiuCentral Laboratory, Ningbo Institute of Innovation for Combined Medicine and Engineering, Ningbo, China.
Jun QiuDepartment of Cardiovascular, Medical College, Ningbo University, Ningbo, China.
Jiangfang LianDepartment of Cardiovascular, Medical College, Ningbo University, Ningbo, China.
Jianqing ZhouDepartment of Cardiovascular, Medical College, Ningbo University, Ningbo, China. zhoujianqing8878@163.com.ORCID 0000-0001-5315-5346
Ningbo University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis, the pathophysiological basis of most malignant cardiovascular diseases, remains a global concern. Transcription factors play a key role in regulating cell function and disease progression in developmental signaling pathways involved in atherosclerosis. Activated transcription factor (ATF) 3 is an adaptive response gene in the ATF/cAMP response element binding (CREB) protein family that acts as a transcription suppressor or activator by forming homodimers or heterodimers with other ATF/CREB members. Appropriate ATF3 expression is vital for normal physiological cell function. Notably, ATF3 exhibits distinct roles in vascular endothelial cells, macrophages, and the liver, which will also be described in detail. This review provides a new perspective for atherosclerosis therapy by summarizing the mechanism of ATF3 in atherosclerosis, as well as the structure and pathophysiological properties of ATF3. KEY MESSAGES: • In endothelial cells, ATF3 overexpression aggravates oxidative stress and inflammation. • In macrophages and liver cells, ATF3 can act as a negative regulator of inflammation and promote cholesterol metabolism. • ATF3 can be used as a potential therapeutic factor in the treatment of atherosclerosis.

Indexed as

Activating Transcription Factor 3AtherosclerosisCholesterolCyclic AMP Response Element-Binding ProteinEndothelial CellsHumansInflammationActivating Transcription Factor 3ATF3 protein, humanCholesterolCyclic AMP Response Element-Binding ProteinAngiogenesisATF3AtherosclerosisEndothelial cell plasticityInflammation

Identifiers

PMID36207452
OpenAlexW4303492420

What Socratic 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 Socratic graph.