ArticleCell death discovery2021
m6A modification promotes miR-133a repression during cardiac development and hypertrophy via IGF2BP2.
Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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.
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.
Who cites it
33 citing papers in PubMed, 55 citations in OpenAlex.
- MicroRNAs in Heart Failure Pathogenesis and Progression: Mechanistic Control, Biomarker Potential, and Translational Perspectives.Life (Basel, Switzerland) · 2026Review
- m6A modification on ncRNAs and underlying mechanisms of exercise in the regulation of pathological cardiac remodeling.European journal of medical research · 2025Review
- Circular RNA circFTO promotes pressure overload-induced cardiac hypertrophy by encoding a novel protein FTO-36aa.Journal of thoracic disease · 2025Article
- METTL14-mediated mActa pharmacologica Sinica · 2025Article
- Reciprocal regulation between m6 A modifications and non-coding RNAs: emerging roles in cancer therapeutic resistance.Discover oncology · 2025Review
- m6A Ribonucleic Acid Methylation in Fibrotic Diseases of Visceral Organs.Small science · 2025Review
- Novel Insight of N6-Methyladenosine in Cardiovascular System.Medicina (Kaunas, Lithuania) · 2025Review
- miRNAs Influence m6A RNA Methylation through FTO and IGF2BP2 in Pressure Overload-Induced Heart Failure.Combinatorial chemistry & high throughput screening · 2025Article
- Regulatory QTLs affecting miRNA-mRNA interactions in cancer: mechanisms, methods, and clinical implications.Frontiers in molecular biosciences · 2025Review
- Non-coding RNAs in heart failure: epigenetic regulatory mechanisms and therapeutic potential.Frontiers in genetics · 2025Review
- Emerging mechanisms and implications of m6A in CVDs: potential applications of natural products.Frontiers in cardiovascular medicine · 2025Review
- Recent advances in methylation modifications of microRNA.Genes & diseases · 2025Review
- Epigenetic regulation of cardiovascular diseases induced by behavioral and environmental risk factors: Mechanistic, diagnostic, and therapeutic insights.FASEB bioAdvances · 2024Review
- The landscape of epigenetic regulation and therapeutic application of NGenes & diseases · 2024Review
- m6A epitranscriptomic and epigenetic crosstalk in cardiac fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Review
- RNA modification-mediated mRNA translation regulation in liver cancer: mechanisms and clinical perspectives.Nature reviews. Gastroenterology & hepatology · 2024Review
- Unlocking the dark matter: noncoding RNAs and RNA modifications in cardiac aging.American journal of physiology. Heart and circulatory physiology · 2024Review
- RNA binding protein IGF2BP2 expression is induced by stress in the heart and mediates dilated cardiomyopathy.Communications biology · 2023Article
- RNA modification in cardiovascular disease: implications for therapeutic interventions.Signal transduction and targeted therapy · 2023Review
- Analysis of the role of glucose metabolism-related genes in dilated cardiomyopathy based on bioinformatics.Journal of thoracic disease · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Both N6-methyladenosine (m6A) RNA modification and microRNAs (miRNAs) are common regulatory mechanisms for gene post-transcription by modulating mRNA stability and translation. They also share the same 3'-untranslated regions (UTRs) regions for their target gene. However, little is known about their potential interaction in cell development and biology. Here, we aimed to investigate how m6A regulates the specific miRNA repression during cardiac development and hypertrophy. Our multiple lines of bioinformatic and molecular biological evidence have shown that m6A modification on cardiac miR-133a target sequence promotes miR-133a repressive effect via AGO2-IGF2BP2 (Argonaute 2-Insulin-like growth factor 2 mRNA binding protein 2) complex. Among 139 cardiac miRNAs, only the seed sequence of miR-133a was inversely complement to m6A consensus motif "GGACH" by sequence alignment analysis. Immunofluorescence staining, luciferase reporter, and m6A-RIP (RNA immunoprecipitation) assays revealed that m6A modification facilitated miR-133a binding to and repressing their targets. The inhibition of the miR-133a on cardiac proliferation and hypertrophy could be prevented by silencing of Fto (FTO alpha-ketoglutarate dependent dioxygenase) which induced m6A modification. IGF2BP2, an m6A binding protein, physically interacted with AGO2 and increased more miR-133a accumulation on its target site, which was modified by m6A. In conclusion, our study revealed a novel and precise regulatory mechanism that the m6A modification promoted the repression of specific miRNA during heart development and hypertrophy. Targeting m6A modification might provide a strategy to repair hypertrophic gene expression induced by miR-133a.
Identifiers
What OpenQuestion holds
Registered trials
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.