Evidence map›Paper›PMID 41744067›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2026

Adenosine-to-Inosine (A-to-I) RNA Editing by ADAR1 to Control RNA Sensing in Cardiovascular Disease.

Chad S Weldy, Jin Billy Li, Thomas Quertermous

Abstract readReview
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 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

3 authors.

Chad S WeldyDepartment of Medicine, Division of Cardiovascular Medicine (C.S.W., T.Q.), Stanford University, CA.ORCID 0000-0003-4652-6422
Jin Billy LiDepartment of Genetics (J.B.L.), Stanford University, CA.ORCID 0000-0003-0713-1399
Thomas QuertermousDepartment of Medicine, Division of Cardiovascular Medicine (C.S.W., T.Q.), Stanford University, CA.ORCID 0000-0002-7645-9067

Funding

Stanford Center for Connecting DNA Variants to Function and PhenotypeUM1HG011972 · NHGRI · STANFORD UNIVERSITY · PI JESSE M ENGREITZ, THOMAS QUERTERMOUS · 2021 to 2026
$10.5M
Causal variant association mechanisms in TCF21 binding coronary disease lociR01HL134817 · NHLBI · STANFORD UNIVERSITY · PI THOMAS QUERTERMOUS · 2017 to 2026
$6.2M
The SMAD3 signaling network in coronary artery disease riskR01HL139478 · NHLBI · STANFORD UNIVERSITY · PI THOMAS QUERTERMOUS · 2018 to 2026
$3.7M
Regulatory and Mechanistic Understanding of ADAR-Mediated RNA EditingR35GM144100 · NIGMS · STANFORD UNIVERSITY · PI Jin Billy Li · 2022 to 2026
$3.2M
Profiling and Dissecting the Dynamic Regulation of RNA EditingR01GM102484 · NIGMS · STANFORD UNIVERSITY · PI LI, JIN BILLY · 2013 to 2021
$3.1M
PDGFD regulates a transcriptional network to modulate smooth muscle cell transition and coronary artery disease riskR01HL156846 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2021 to 2024
$2.7M
Identifying tobacco-genetic interactions through study of the aryl hydrocarbon receptor pathway.R01HL151535 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2021 to 2024
$2.7M
Systematic characterization of trans regulation of A-to-I RNA editing in neuronsR01MH115080 · NIMH · STANFORD UNIVERSITY · PI LI, JIN BILLY · 2017 to 2021
$2.3M
Systematic identification and characterization of immunogenic double-stranded RNAsR01AI182437 · NIAID · STANFORD UNIVERSITY · PI Jin Billy Li · 2024 to 2026
$2.1M
LncRNA Transcriptional Mechanisms of Coronary Artery Disease RiskR01HL145708 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2019 to 2022
$1.6M
ADAR mediated RNA editing is a causal mechanism in coronary artery diseaseK08HL167699 · NHLBI · STANFORD UNIVERSITY · PI Chad S Weldy · 2023 to 2026
$664k
NHGRI NIH HHS UM1 HG011972NHLBI NIH HHS K08 HL167699NHLBI NIH HHS L30 HL159413NHLBI NIH HHS R01 HL134817NHLBI NIH HHS R01 HL139478NHLBI NIH HHS R01 HL145708NHLBI NIH HHS R01 HL151535NHLBI NIH HHS R01 HL156846NIAID NIH HHS R01 AI182437NIGMS NIH HHS R01 GM102484NIGMS NIH HHS R35 GM144100NIMH NIH HHS R01 MH115080
6 · The paper itself

Abstract

Across biology, organisms have retained a mechanism to diversify the RNA transcriptome through RNA editing. Mediated by ADAR (adenosine deaminase acting on RNA) enzymes, Adenosines in double-stranded RNA (dsRNA) structures can be edited to Inosines (adenosine-to-inosine edit). Although this can change the amino acid sequence if it occurs in a coding sequence of mRNA, the majority of RNA editing in mammalian cells is found in noncoding repetitive elements. These repetitive elements have a predisposition to form long dsRNA structures that can mimic a dsRNA virus. Since the initial discoveries of RNA editing over 30 years ago, investigators have now identified ADAR1 to play a crucial role in suppressing innate immune activation and type I interferon signaling. Through adenosine-to-inosine editing, these dsRNA change their conformational structures and evade activation of the innate immune dsRNA sensor, MDA5 (melanoma differentiation-associated gene 5; gene symbol

Indexed as

AdenosineAdenosine DeaminaseCardiovascular DiseasesInosineRNA-Binding ProteinsRNA, Double-StrandedRNA EditingAnimalsGenetic Predisposition to DiseaseHumansImmunity, InnateInnate Immunity RecognitionInterferon-Induced Helicase, IFIH1Signal TransductionADAR protein, humanAdenosineAdenosine DeaminaseIFIH1 protein, humanInosineInterferon-Induced Helicase, IFIH1RNA-Binding ProteinsRNA, Double-Strandedadenosine deaminasecardiovascular diseasescoronary artery diseaseRNA, double-strandedRNA editing

Identifiers

PMID41744067
PMCPMC12948147

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.