Evidence map›Paper›PMID 39858624›Full record

ReviewGenes2025

ADAR Therapeutics as a New Tool for Personalized Medicine.

Matteo Bertoli, Luca La Via, Alessandro Barbon

Abstract readReview
In one paragraph

Review in Genes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Review
  5. 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

3 authors.

Matteo BertoliDepartment of Molecular and Translational Medicine, University of Brescia, 25123 Brescia, Italy.
Luca La ViaDepartment of Molecular and Translational Medicine, University of Brescia, 25123 Brescia, Italy.ORCID 0000-0002-8475-1551
Alessandro BarbonDepartment of Molecular and Translational Medicine, University of Brescia, 25123 Brescia, Italy.ORCID 0000-0002-1127-7764

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the field of RNA therapy, innovative approaches based on adenosine deaminases acting on RNA (ADAR)-mediated site-directed RNA editing (SDRE) have been established, providing an exciting opportunity for RNA therapeutics. ADAR1 and ADAR2 enzymes are accountable for the predominant form of RNA editing in humans, which involves the hydrolytic deamination of adenosine (A) to inosine (I). This inosine is subsequently interpreted as guanosine (G) by the translational and splicing machinery because of their structural similarity. Intriguingly, the novel SDRE system leverages this recoding ability of ADAR proteins to correct the pathogenic G to A nucleotide mutations through a short, engineered guide RNA (gRNA). Thus, ADAR-mediated SDRE is emerging as a powerful tool to manipulate the genetic information at the RNA level and correct disease-causing mutations without causing damage to the genome. Further it is emerging as a new instrument for personalized medicine, since treatments can be tailored to the unique genetic mutations present in an individual patient. In this short review, we aimed to described the main approached bases on ADARs activity, highlighting their advantages and disadvantages.

Indexed as

Adenosine DeaminasePrecision MedicineRNA-Binding ProteinsRNA EditingAnimalsHumansMutationADAR protein, humanAdenosine DeaminaseRNA-Binding ProteinsADAR1ADAR2RNA editingRNA therapeuticsSDRE

Identifiers

PMID39858624
PMCPMC11764986

What OpenQuestion holds

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Registered trials

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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.