Evidence map›Paper›PMID 42523702›Full record

ReviewFrontiers in molecular biosciences2026

The RNA-binding protein CELF4: from molecular regulatory networks to clinical translation in cross-system diseases.

Qingsong Wang, Wenlong Yue, Dan Lin, Xianmin Wang, Tongyong Luo, Jun Yin

Abstract readReview
In one paragraph

Review in Frontiers in molecular biosciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

6 authors.

Qingsong Wang *Department of Pediatrics, West China Hospital Sichuan University Jintang Hospital. Jintang First People's Hospital, Chengdu, Sichuan, China.
Wenlong Yue *Department of Neurosurgery, West China Hospital Sichuan University Jintang Hospital. Jintang First People's Hospital, Chengdu, Sichuan, China.
Dan LinDepartment of Internal Medicine, Guancang Community Health Service Center, Chengdu, Sichuan, China.
Xianmin WangPediatric Cardiology Center, Sichuan Provincial Women's and Children's Hospital, The Affiliated Women's and Children's Hospital of Chengdu Medical College, Chengdu, Sichuan, China.
Tongyong LuoPediatric Cardiology Center, Sichuan Provincial Women's and Children's Hospital, The Affiliated Women's and Children's Hospital of Chengdu Medical College, Chengdu, Sichuan, China.
Jun YinDepartment of Ultrasound, West China Hospital Sichuan University Jintang Hospital. Jintang First People's Hospital, Chengdu, Sichuan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CELF4 (CUGBP Elav-like family member 4), encoded by the human chromosome 18q12.2 locus, is an RNA-binding protein that recognizes UG-rich sequences within the 3'untranslated region (3'UTR) of target mRNAs to regulate splicing, stability, and local translation at the post-transcriptional level. Under physiological conditions, CELF4 exerts translational repression during synaptic development in the central nervous system (CNS), maintains excitatory homeostasis, and sets peripheral sensory thresholds; in cardiac fibroblasts, it is expressed at low levels and restricts baseline TGF-β signaling. In pathological states, CELF4 exhibits context-dependent bidirectional modulation: in autism spectrum disorder (ASD), major depressive disorder (MDD), epilepsy, chronic pain, and endometrial cancer, its downregulation or epigenetic silencing causes translational derepression of target mRNAs; in cardiac fibrosis, TGF-β1-induced upregulation suppresses FMO2 translation and activates the Smad2/3 pathway. Additionally, pleiotropic genetic loci near CELF4 have been linked to gut-brain axis comorbidities and obesity-hypertension syndromes. Clinically, CELF4 promoter methylation testing has entered validation trials for non-invasive endometrial cancer screening, and its haploinsufficiency has been incorporated into the genetic diagnosis of 18q12.2 microdeletion syndrome; pharmacological and gene-replacement strategies targeting CELF4 remain at the preclinical proof-of-concept stage. Here, we review the molecular regulatory networks of CELF4 and its mechanisms across multisystem diseases, discuss the current status and limitations of clinical translation, and may guide future research on diagnostic biomarkers and therapeutic strategies targeting this protein.

Indexed as

cardiac fibrosisCelf4precision medicineRNA-binding proteinsynaptic homeostasistranslational repression

Identifiers

PMID42523702
PMCPMC13407360

What Socratic 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 Socratic graph.