ArticleJournal of molecular cell biology2026
egr1 and egr4 regulate zebrafish renal regeneration by promoting foxm1 expression.
Article in Journal of molecular cell biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- A comparative transcriptomics analysis of mammalian and non-mammalian acute kidney injury (AKI) models.Frontiers in cell and developmental biology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Early growth response (Egr) factors are involved in tissue development and repair. However, few studies have focused on the role of egr genes in renal regeneration after acute kidney injury (AKI) and the underlying mechanisms. In this study, we observed that egr1 and egr4 were sharply upregulated in wild type zebrafish at 1 day post-injury by gentamicin. Further experiments with egr1 and egr4 mutants showed that egr1 and egr4 were involved in zebrafish renal regeneration after AKI by regulating the proliferation and apoptosis of tubular cells. foxm1 is expressed in injured kidneys and involved in kidney repair. Loss of foxm1 inhibited zebrafish renal regeneration by decreasing the proliferation and increasing the apoptosis of tubular cells. Moreover, Egr1 and Egr4 promoted foxm1 expression by directly binding to the foxm1 promoter, thus regulating renal regeneration. Our results revealed that the rapid and transient induction of egr1 and egr4 after AKI exerts a renoprotective role through upregulating foxm1 to facilitate kidney regeneration. Therefore, the egr1/egr4-foxm1 regulatory axis holds a therapeutic potential for the treatment of AKI.
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.