Evidence map›Paper›PMID 40065061›Full record

ArticleScientific reports2025

Activation of endogenous retroviruses characterizes the maternal-fetal interface in the BTBR mouse model of autism spectrum disorder.

Chiara Cipriani, Antonella Camaioni, Anna Maria Tartaglione, Martina Giudice, Allegra Conti, Vita Petrone, Martino Tony Miele, Claudia Matteucci, Enrico Garaci, Gemma Calamandrei and 4 more

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In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

14 authors.

Chiara CiprianiDepartment of Experimental Medicine, University of Rome Tor Vergata, Via Montpellier, 1, 00133, Rome, Italy. chiara.cipriani@uniroma2.it.
Antonella CamaioniDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, Rome, Italy.
Anna Maria TartaglioneCentre for Behavioural Sciences and Mental Health, Istituto Superiore Di Sanità, Rome, Italy.
Martina GiudiceDepartment of Experimental Medicine, University of Rome Tor Vergata, Via Montpellier, 1, 00133, Rome, Italy.
Allegra ContiDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, Rome, Italy.
Vita PetroneDepartment of Experimental Medicine, University of Rome Tor Vergata, Via Montpellier, 1, 00133, Rome, Italy.
Martino Tony MieleDepartment of Experimental Medicine, University of Rome Tor Vergata, Via Montpellier, 1, 00133, Rome, Italy.
Claudia MatteucciDepartment of Experimental Medicine, University of Rome Tor Vergata, Via Montpellier, 1, 00133, Rome, Italy.
Enrico GaraciIRCCS San Raffaele Pisana, Rome, Italy.
Gemma CalamandreiCentre for Behavioural Sciences and Mental Health, Istituto Superiore Di Sanità, Rome, Italy.
Nicola ToschiDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, Rome, Italy.
Paola Sinibaldi-VallebonaDepartment of Experimental Medicine, University of Rome Tor Vergata, Via Montpellier, 1, 00133, Rome, Italy.
Laura RicceriCentre for Behavioural Sciences and Mental Health, Istituto Superiore Di Sanità, Rome, Italy.
Emanuela BalestrieriDepartment of Experimental Medicine, University of Rome Tor Vergata, Via Montpellier, 1, 00133, Rome, Italy.

Funding

Istituto Superiore di Sanità ISS 13/cal 508
6 · The paper itself

Abstract

Endogenous retroviruses (ERVs) are genetic elements derived from a process of germline infection by exogenous retroviruses. Some ERVs have been co-opted for physiological functions, and their activation has been associated with complex diseases, including Autism Spectrum Disorder (ASD). We have already demonstrated an abnormal expression of ERVs in the BTBR T + tf/J (BTBR) mouse model of ASD during intrauterine life till adulthood. Thus, starting from the assumptions that ERVs may contribute to the derailment of neurodevelopment and that ASD has fetal origins as a consequence of adverse intrauterine conditions, the present study aims to characterize the transcriptional activity of selected ERVs (MusD, IAP, Syn-A, Syn-B, ARC and GLN), LINE-1, inflammatory mediators (IL-6, IL-10, IL-11 CXCL-1) at the maternal-fetal interface and in dissected embryos from BTBR mice. Our results highlight the deregulation of ERVs and inflammatory mediators at the maternal-fetal interface, and in cephalic and non-cephalic embryonic tissues from BTBR compared to C57BL/6 J. Several correlations among ERV expression levels emerged in different tissues from C57BL/6 J mice while, in BTBR mice, no correlations were found, suggesting that in this model, the acquisition of autistic-like traits might be linked to the dysregulation of ERV activity occurring during intra-uterine life.

Indexed as

Autism Spectrum DisorderEndogenous RetrovirusesMaternal-Fetal ExchangeAnimalsDisease Models, AnimalFemaleMaleMiceMice, Inbred C57BLPregnancyAutism Spectrum DisorderBTBREndogenous retrovirusesERVInflammationMaternal–fetal interface

Identifiers

PMID40065061
PMCPMC11894120

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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.