Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (689 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A process that changes the nucleotide sequence of mRNA from that of the DNA template encoding it. Some major classes of RNA editing are as follows: 1, the conversion of cytosine to uracil in mRNA; 2, the addition of variable number of guanines at pre-determined sites; and 3, the addition and deletion of uracils, templated by guide-RNAs (RNA, guide, kinetoplastida).
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Editing, RNA; Editings, RNA; RNA Editings; RNA, Messenger, Editing.
Where it fits in the MeSH classification
- Broader topics
- RNA Processing, Post-Transcriptional
Related concepts
- Guide
- Kinetoplastida
Research landscape
PubMed indexes 4,899 records tagged with the MeSH heading “RNA Editing” (counts retrieved 2026-10-29). 1,272 of them (26.0%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 1,873 records.
Reviews account for 827 records (16.9%) and meta-analyses for 3. Randomized controlled trials number 1 (0.0%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 565 |
| 2000-2009 | 1,189 |
| 2010-2019 | 1,873 |
| 2020 onward | 1,272 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 827 | 16.9% |
| Meta-analyses | 3 | 0.1% |
| Randomized controlled trials | 1 | 0.0% |
Method: PubMed query "RNA Editing"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in molecular biology
Molecular biology establishes mechanisms through controlled experiments, often in simplified systems such as purified proteins, cultured cells or model organisms. Such work can show what is possible in a defined system, but whether a pathway matters in a whole organism or in human disease needs further evidence. Check the experimental system, whether findings were reproduced by independent groups, and whether the authors tested the mechanism directly or inferred it from correlation.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Deciphering miRNAs' Action through miRNA Editing | 2019 | Review article Design not recorded in structured metadata | 641 | cc by PMID 31835747 · DOI · PMC6941098 |
| Assessing and advancing the safety of CRISPR-Cas tools: from DNA to RNA editing | 2023 | Review article Design not recorded in structured metadata | 159 | cc by PMID 36639728 · DOI · PMC9838544 |
| ADAR1 RNA editing enzyme regulates R-loop formation and genome stability at telomeres in cancer cells | 2021 | Research article Design not recorded in structured metadata | 123 | cc by PMID 33712600 · DOI · PMC7955049 |
| Enhancing RNA base editing on mammalian transcripts with small nuclear RNAs | 2026 | Research article Design not recorded in structured metadata | 5 | cc by PMID 40968292 · DOI · PMC13003931 |
Deciphering miRNAs' Action through miRNA Editing [1]
Abstract reading summary — source excerpts
- Opening excerpt
- MicroRNAs (miRNAs) are small non-coding RNAs with the capability of modulating gene expression at the post-transcriptional level either by inhibiting messenger RNA (mRNA) translation or by promoting mRNA degradation.
- Closing excerpt
- Herein, we will discuss the current knowledge on miRNA editing and how this mechanism regulates miRNA biogenesis and activity.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (286 words)
MicroRNAs (miRNAs) are small non-coding RNAs with the capability of modulating gene expression at the post-transcriptional level either by inhibiting messenger RNA (mRNA) translation or by promoting mRNA degradation. The outcome of a myriad of physiological processes and pathologies, including cancer, cardiovascular and metabolic diseases, relies highly on miRNAs. However, deciphering the precise roles of specific miRNAs in these pathophysiological contexts is challenging due to the high levels of complexity of their actions. Indeed, regulation of mRNA expression by miRNAs is frequently cell/organ specific; highly dependent on the stress and metabolic status of the organism; and often poorly correlated with miRNA expression levels. Such biological features of miRNAs suggest that various regulatory mechanisms control not only their expression, but also their activity and/or bioavailability. Several mechanisms have been described to modulate miRNA action, including genetic polymorphisms, methylation of miRNA promoters, asymmetric miRNA strand selection, interactions with RNA-binding proteins (RBPs) or other coding/non-coding RNAs. Moreover, nucleotide modifications (A-to-I or C-to-U) within the miRNA sequences at different stages of their maturation are also critical for their functionality. This regulatory mechanism called "RNA editing" involves specific enzymes of the adenosine/cytidine deaminase family, which trigger single nucleotide changes in primary miRNAs. These nucleotide modifications greatly influence a miRNA's stability, maturation and activity by changing its specificity towards target mRNAs. Understanding how editing events impact miRNA's ability to regulate stress responses in cells and organs, or the development of specific pathologies, e.g., metabolic diseases or cancer, should not only deepen our knowledge of molecular mechanisms underlying complex diseases, but can also facilitate the design of new therapeutic approaches based on miRNA targeting. Herein, we will discuss the current knowledge on miRNA editing and how this mechanism regulates miRNA biogenesis and activity.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31835747 · DOI · PMC6941098
Assessing and advancing the safety of CRISPR-Cas tools: from DNA to RNA editing [2]
Abstract reading summary — source excerpts
- Opening excerpt
- CRISPR-Cas gene editing has revolutionized experimental molecular biology over the past decade and holds great promise for the treatment of human genetic diseases.
- Closing excerpt
- We summarize the capabilities and limitations of each CRISPR tool from DNA editing to RNA editing, and highlight the opportunities for future improvements and applications in basic research, as well as the therapeutic and clinical considerations for their use in patients.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (101 words)
CRISPR-Cas gene editing has revolutionized experimental molecular biology over the past decade and holds great promise for the treatment of human genetic diseases. Here we review the development of CRISPR-Cas9/Cas12/Cas13 nucleases, DNA base editors, prime editors, and RNA base editors, focusing on the assessment and improvement of their editing precision and safety, pushing the limit of editing specificity and efficiency. We summarize the capabilities and limitations of each CRISPR tool from DNA editing to RNA editing, and highlight the opportunities for future improvements and applications in basic research, as well as the therapeutic and clinical considerations for their use in patients.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36639728 · DOI · PMC9838544
ADAR1 RNA editing enzyme regulates R-loop formation and genome stability at telomeres in cancer cells [3]
Abstract reading summary — source excerpts
- Opening excerpt
- ADAR1 is involved in adenosine-to-inosine RNA editing.
- Closing excerpt
- This ADAR1p110-dependent control of telomeric R-loops is required for continued proliferation of telomerase-reactivated cancer cells, revealing the pro-oncogenic nature of ADAR1p110 and identifying ADAR1 as a promising therapeutic target of telomerase positive cancers.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (149 words)
ADAR1 is involved in adenosine-to-inosine RNA editing. The cytoplasmic ADAR1p150 edits 3'UTR double-stranded RNAs and thereby suppresses induction of interferons. Loss of this ADAR1p150 function underlies the embryonic lethality of Adar1 null mice, pathogenesis of the severe autoimmune disease Aicardi-Goutières syndrome, and the resistance developed in cancers to immune checkpoint blockade. In contrast, the biological functions of the nuclear-localized ADAR1p110 remain largely unknown. Here, we report that ADAR1p110 regulates R-loop formation and genome stability at telomeres in cancer cells carrying non-canonical variants of telomeric repeats. ADAR1p110 edits the A-C mismatches within RNA:DNA hybrids formed between canonical and non-canonical variant repeats. Editing of A-C mismatches to I:C matched pairs facilitates resolution of telomeric R-loops by RNase H2. This ADAR1p110-dependent control of telomeric R-loops is required for continued proliferation of telomerase-reactivated cancer cells, revealing the pro-oncogenic nature of ADAR1p110 and identifying ADAR1 as a promising therapeutic target of telomerase positive cancers.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33712600 · DOI · PMC7955049
Enhancing RNA base editing on mammalian transcripts with small nuclear RNAs [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Endogenous uridine-rich small nuclear RNAs (U snRNAs) form RNA-protein complexes to process eukaryotic pre-mRNA into mRNA.
- Closing excerpt
- Our results advance the endogenous protein-mediated RNA base editing toolbox and RNA-targeting technologies to treat genetic diseases.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (153 words)
Endogenous uridine-rich small nuclear RNAs (U snRNAs) form RNA-protein complexes to process eukaryotic pre-mRNA into mRNA. Previous studies have demonstrated programmable U snRNA guide-targeted exon inclusion and exclusion. Here we investigated whether snRNAs can also enhance RNA base editing over state-of-the-art RNA-targeting technologies in human cells. Compared with adenosine deaminase acting on RNA (ADAR)-recruiting circular RNAs, we find that guided A>I snRNAs consistently increase adenosine-to-inosine editing for higher exon count genes, perturb substantially fewer off-target genes and localize more persistently to the nucleus where ADAR is expressed. A>I snRNAs also more efficiently edit long noncoding RNAs and pre-mRNA 3' splice sites to promote splicing changes. Lastly, snRNA-H/ACA box snoRNA fusions (U>Ψ snRNAs) increase targeted RNA pseudouridylation without DKC1 overexpression, facilitating improved CFTR rescue from nonsense-mediated mRNA decay in a cystic fibrosis human bronchial epithelial cell model. Our results advance the endogenous protein-mediated RNA base editing toolbox and RNA-targeting technologies to treat genetic diseases.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40968292 · DOI · PMC13003931
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Functions and regulation of RNA editing by ADAR deaminases [5]
- Research article RNA editing by adenosine deaminases that act on RNA [6]
- Research article A-to-I editing of coding and non-coding RNAs by ADARs [7]
- Research article Beyond editing: repurposing CRISPR-Cas9 for precision genome regulation and interrogation [8]
- Research article A-to-I RNA editing - immune protector and transcriptome diversifier [9]
- Research article CRISPR/Cas9 for genome editing: progress, implications and challenges [10]
References
- Correia de Sousa M, Gjorgjieva M, Dolicka D, Sobolewski C, Foti M. Deciphering miRNAs' Action through miRNA Editing. . 2019. PMID 31835747 · DOI · PMC6941098
- Tao J, Bauer DE, Chiarle R. Assessing and advancing the safety of CRISPR-Cas tools: from DNA to RNA editing. . 2023. PMID 36639728 · DOI · PMC9838544
- Shiromoto Y, Sakurai M, Minakuchi M, Ariyoshi K, Nishikura K. ADAR1 RNA editing enzyme regulates R-loop formation and genome stability at telomeres in cancer cells. . 2021. PMID 33712600 · DOI · PMC7955049
- Smargon AA, Pant D, Gomberg TA, Fagre C, Glynne S, Nguyen J, et al.. Enhancing RNA base editing on mammalian transcripts with small nuclear RNAs. . 2026. PMID 40968292 · DOI · PMC13003931
- Nishikura K. Functions and regulation of RNA editing by ADAR deaminases. Annu Rev Biochem. 2010. PMID 20192758 · DOI · PMC2953425
- Bass BL. RNA editing by adenosine deaminases that act on RNA. Annu Rev Biochem. 2002. PMID 12045112 · DOI · PMC1823043
- Nishikura K. A-to-I editing of coding and non-coding RNAs by ADARs. Nat Rev Mol Cell Biol. 2016. PMID 26648264 · DOI · PMC4824625
- Dominguez AA, Lim WA, Qi LS. Beyond editing: repurposing CRISPR-Cas9 for precision genome regulation and interrogation. Nat Rev Mol Cell Biol. 2016. PMID 26670017 · DOI · PMC4922510
- Eisenberg E, Levanon EY. A-to-I RNA editing - immune protector and transcriptome diversifier. Nat Rev Genet. 2018. PMID 29692414 · DOI
- Zhang F, Wen Y, Guo X. CRISPR/Cas9 for genome editing: progress, implications and challenges. Hum Mol Genet. 2014. PMID 24651067 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.