Evidence map›Paper›PMID 36299447›Full record

ReviewResearch (Washington, D.C.)2022

CCAAT/Enhancer-Binding Proteins in Fibrosis: Complex Roles Beyond Conventional Understanding.

Lexun Wang, Jiaojiao Feng, Yanyue Deng, Qianqian Yang, Quxing Wei, Dewei Ye, Xianglu Rong, Jiao Guo

Open access · goldAbstract readReview
In one paragraph

Review in Research (Washington, D.C.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. THSD7A Exacerbates Atherosclerosis via Activation of Signaling Axis αvβ3/CEBPD/IL1A.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  14. CEBPB dampens the cuproptosis sensitivity of colorectal cancer cells by facilitating the PI3K/AKT/mTOR signaling pathway.Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology Association · 2024
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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

8 authors at 1 institution in 1 country.

Lexun WangGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine, China.ORCID https://orcid.org/0000-0002-7476-6645
Jiaojiao FengGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine, China.
Yanyue DengGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine, China.
Qianqian YangGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine, China.
Quxing WeiGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine, China.
Dewei YeGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine, China.
Xianglu RongGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine, China.
Jiao GuoGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine, China.ORCID https://orcid.org/0000-0002-0050-5055
Ministry of Education of the People's Republic of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CCAAT/enhancer-binding proteins (C/EBPs) are a family of at least six identified transcription factors that contain a highly conserved basic leucine zipper domain and interact selectively with duplex DNA to regulate target gene expression. C/EBPs play important roles in various physiological processes, and their abnormal function can lead to various diseases. Recently, accumulating evidence has demonstrated that aberrant C/EBP expression or activity is closely associated with the onset and progression of fibrosis in several organs and tissues. During fibrosis, various C/EBPs can exert distinct functions in the same organ, while the same C/EBP can exert distinct functions in different organs. Modulating C/EBP expression or activity could regulate various molecular processes to alleviate fibrosis in multiple organs; therefore, novel C/EBPs-based therapeutic methods for treating fibrosis have attracted considerable attention. In this review, we will explore the features of C/EBPs and their critical functions in fibrosis in order to highlight new avenues for the development of novel therapies targeting C/EBPs.

Identifiers

PMID36299447
PMCPMC9575473
OpenAlexW4303475878

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.