Evidence map›Paper›PMID 42193920›Full record

ArticleCells2026

The miR-1843a-3p/

Yunwei Shi, Hong Wang, Nur Salihah Lau, Amanda Tan Ying Xin, Caiping Wang, Feng Ru Tang

Abstract read
In one paragraph

Article in Cells, 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.

Yunwei ShiJiangsu Key Laboratory of Tissue Engineering and Neuroregeneration, Key Laboratory of Neuroregeneration of Ministry of Education, Co-Innovation Center of Neuroregeneration, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Nantong University, Nantong 226001, China.ORCID 0009-0000-3374-8734
Hong WangRadiation Physiology Laboratory, Singapore Nuclear Research and Safety Institute, National University of Singapore, 16 Prince George's Park, #03-03, Singapore 118415, Singapore.
Nur Salihah LauRadiation Physiology Laboratory, Singapore Nuclear Research and Safety Institute, National University of Singapore, 16 Prince George's Park, #03-03, Singapore 118415, Singapore.ORCID 0009-0009-2447-0051
Amanda Tan Ying XinRadiation Physiology Laboratory, Singapore Nuclear Research and Safety Institute, National University of Singapore, 16 Prince George's Park, #03-03, Singapore 118415, Singapore.ORCID 0009-0009-4863-6386
Caiping WangJiangsu Key Laboratory of Tissue Engineering and Neuroregeneration, Key Laboratory of Neuroregeneration of Ministry of Education, Co-Innovation Center of Neuroregeneration, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Nantong University, Nantong 226001, China.
Feng Ru TangRadiation Physiology Laboratory, Singapore Nuclear Research and Safety Institute, National University of Singapore, 16 Prince George's Park, #03-03, Singapore 118415, Singapore.ORCID 0000-0003-2462-1787

Funding

National Research Foundation of Singapore Block grant
6 · The paper itself

Abstract

Prenatal exposure to ionizing radiation is a known risk factor for neurodevelopmental deficits; however, the molecular mechanisms linking chronic embryonic insult to abnormal brain development remain poorly understood. This study investigated the long-term consequences of chronic prenatal gamma irradiation throughout gestation in C57BL/6 mice. Behavioural analysis of adult offspring revealed a specific increase in depression-like behaviours, with no significant alterations in anxiety or general exploratory activity. Immunohistochemical assessment demonstrated a significant reduction in adult hippocampal neurogenesis, marked by decreased doublecortin (DCX)-positive newborn neurons in the subgranular zone and fewer NeuN-positive mature neurons in the dentate gyrus hilus. Integrated RNA-seq, qPCR, and Western blot analyses implicated the upregulation of the Mef2c/Egr1 signalling pathway in this neurogenic deficit. Furthermore, miRNA sequencing identified a pronounced decrease in miR-1843a-3p, which was subsequently validated to directly target Mef2c. Collectively, these findings suggest that prenatal gamma irradiation disrupts neurogenic processes and adult brain function, leading to specific behavioral abnormalities. This long-term impairment is associated with, and may be at least partially mediated by, dysregulation of the miR-1843a-3p/Mef2c/Egr1 pathway.

Indexed as

Behavior, AnimalEarly Growth Response Protein 1Gamma RaysHippocampusMEF2 Transcription FactorsMicroRNAsNeurogenesisPrenatal Exposure Delayed EffectsAnimalsDoublecortin ProteinFemaleMaleMiceMice, Inbred C57BLNeuronsPregnancyDcx protein, mouseDoublecortin ProteinEarly Growth Response Protein 1Egr1 protein, mouseMef2c protein, mouseMEF2 Transcription FactorsMicroRNAsbehavioural abnormalitiesEgr1Mef2cmiR-1843a-3pneurogenesisprenatal gamma irradiation

Identifiers

PMID42193920
PMCPMC13205106

What OpenQuestion holds

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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.