Evidence map›Paper›PMID 38383514›Full record

ArticleCell death & disease2024

Transcription of endogenous retroviruses in senescent cells contributes to the accumulation of double-stranded RNAs that trigger an anti-viral response that reinforces senescence.

Eros Di Giorgio, Liliana Ranzino, Vanessa Tolotto, Emiliano Dalla, Matteo Burelli, Nicolò Gualandi, Claudio Brancolini

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
5.1field-weighted citation impact, top 4% of its field
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

19 citing papers in PubMed, 21 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

Eros Di GiorgioLaboratory of Biochemistry, Department of Medicine, Università degli Studi di Udine, p.le Kolbe 4, 33100, Udine, Italy.
Liliana RanzinoLaboratory of Epigenomics, Department of Medicine, Università degli Studi di Udine, p.le Kolbe 4, 33100, Udine, Italy.
Vanessa TolottoLaboratory of Epigenomics, Department of Medicine, Università degli Studi di Udine, p.le Kolbe 4, 33100, Udine, Italy.ORCID 0000-0002-3619-4981
Emiliano DallaLaboratory of Epigenomics, Department of Medicine, Università degli Studi di Udine, p.le Kolbe 4, 33100, Udine, Italy.
Matteo BurelliLaboratory of Biochemistry, Department of Medicine, Università degli Studi di Udine, p.le Kolbe 4, 33100, Udine, Italy.
Nicolò GualandiLaboratory of Epigenomics, Department of Medicine, Università degli Studi di Udine, p.le Kolbe 4, 33100, Udine, Italy.
Claudio BrancoliniLaboratory of Epigenomics, Department of Medicine, Università degli Studi di Udine, p.le Kolbe 4, 33100, Udine, Italy. claudio.brancolini@uniud.it.ORCID 0000-0002-6597-5373
University of Udine · IT

Funding

Associazione Italiana per la Ricerca sul Cancro (Italian Association for Cancer Research) IG 2021 - ID. 26200Associazione Italiana per la Ricerca sul Cancro (Italian Association for Cancer Research) MFAG 2020- ID. 25000
6 · The paper itself

Abstract

An important epigenetic switch marks the onset and maintenance of senescence. This allows transcription of the genetic programs that arrest the cell cycle and alter the microenvironment. Transcription of endogenous retroviruses (ERVs) is also a consequence of this epigenetic switch. In this manuscript, we have identified a group of ERVs that are epigenetically silenced in proliferating cells but are upregulated during replicative senescence or during various forms of oncogene-induced senescence, by RAS and Akt, or after HDAC4 depletion. In a HDAC4 model of senescence, removal of the repressive histone mark H3K27me3 is the plausible mechanism that allows the transcription of intergenic ERVs during senescence. We have shown that ERVs contribute to the accumulation of dsRNAs in senescence, which can initiate the antiviral response via the IFIH1-MAVS signaling pathway and thus contribute to the maintenance of senescence. This pathway, and MAVS in particular, plays an active role in shaping the microenvironment and maintaining growth arrest, two essential features of the senescence program.

Indexed as

Endogenous RetrovirusesHistonesAntiviral AgentsCellular SenescenceEpigenesis, GeneticAntiviral AgentsHistones

Identifiers

PMID38383514
PMCPMC10882003
OpenAlexW4391999457

What OpenQuestion 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 OpenQuestion graph.