ArticleBMC cardiovascular disorders2025
CUGBP Elav-like family member 4 promotes cardiac remodeling through Inhibition of FMO2.
Article in BMC cardiovascular disorders, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.
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.
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.
Who cites it
3 citing papers in PubMed.
- CELF family of RNA-binding proteins: roles in disease biology and potential for therapeutic intervention.Cell communication and signaling : CCS · 2026Review
- The RNA-binding protein CELF4: from molecular regulatory networks to clinical translation in cross-system diseases.Frontiers in molecular biosciences · 2026Review
- Correction: CUGBP Elav-like family member 4 promotes cardiac remodeling through inhibition of FMO2.BMC cardiovascular disorders · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors.
Funding
Abstract
backgroundCardiac fibrosis exerts a lasting influence on the development of heart failure (HF), whereas there is no specific and effective therapeutic strategy to combat cardiac fibrosis.
objectivesCUGBP Elav-like family member 4 (CELF4), an RNA-binding protein, influences tumor progression through post-transcription regulation, while the role of CELF4 in HF remains elusive.
methodsTransverse aortic constriction (TAC) was applied to induce pressure overload-induced cardiac remodeling in 6-week-old male mice. Global CELF4 knockout (CELF4
resultsThe mRNA expression of CELF4 was significantly upregulated in mouse failing heart after TAC. In vitro experiments showed that CELF4 was specifically induced by TGF-β1 in CFs, but no change was observed in cardiomyocytes. CELF4 deficiency attenuated cardiac fibrosis and preserved the functions of pressure overload-induced hearts. We observed that depletion of CELF4 markedly reduced CF proliferation and migration induced by TGF-β1. Furthermore, depletion of CELF4 alleviated Collagen I and α-SMA expression in CFs as determined by western blots. Using RNA pull-down and Luciferase assay, we found an intrinsic binding of CELF4 with 3'UTR of flavin containing monooxygenase 2 (FMO2), which blunted the phosphorylation of Smad2/3 in CFs after TGF-β1 stimulation.
conclusionOur study delineates that decreased CELF4 retards cardiac fibrosis and HF via interaction with FMO2 and suppression of Smad2/3 signaling. Inhibition of CELF4 may become a potential therapy target for cardiac fibrosis and HF.
Indexed as
Identifiers
What Socratic holds
Registered trials
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.