ArticleAnnals of translational medicine2019
Increased m6A methylation level is associated with the progression of human abdominal aortic aneurysm.
Article in Annals of translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.
- RNA methylation in vascular disease: a systematic review.Journal of cardiothoracic surgery · 2022Pooled it
- N6-methyladenosine (m6A) post-transcriptional modification regulation of mRNA, an overlooked therapeutic opportunity to leverage mRNA processing in vascular smooth muscle cells.Vascular pharmacology · 2026Review
- mScientific reports · 2026Article
- N6-methyladenosine (miScience · 2026Article
- The mechanism of m6A modification in cardiovascular diseases: A systematic review.Genes & diseases · 2026Review
- Current Insights into Obesity and mBiomedicines · 2025Review
- The role of m6A methylation in abdominal aortic aneurysms: Mechanisms, progress and future perspectives (Review).Molecular medicine reports · 2025Review
- METTL3: a multifunctional regulator in diseases.Molecular and cellular biochemistry · 2025Review
- Altered expression and potential role of N6-methyladenosine mRNA methylation in abdominal aortic aneurysm mouse model.Scientific reports · 2025Article
- Epitranscriptome: A Novel Regulatory Layer during Atherosclerosis Progression.Current medicinal chemistry · 2025Review
- Cross-talk of mFrontiers in immunology · 2025Article
- Biogenesis of circRBM33 mediated by N6-methyladenosine and its function in abdominal aortic aneurysm.Epigenetics · 2024Article
- Differentiation and Growth-Arrest-Related lncRNA (International journal of molecular sciences · 2024Article
- Review
- NAging and disease · 2024Review
- The role of m6A in angiogenesis and vascular diseases.iScience · 2024Review
- N6-methyladenosine in myeloid cells: a novel regulatory factor for inflammation-related diseases.Journal of physiology and biochemistry · 2024Review
- N6-methyladenosine-associated genetic variants in NECTIN2 and HPCAL1 are risk factors for abdominal aortic aneurysm.iScience · 2024Article
- Colchicine Blocks Abdominal Aortic Aneurysm Development by Maintaining Vascular Smooth Muscle Cell Homeostasis.International journal of biological sciences · 2024Article
- Epigenetic modifications in abdominal aortic aneurysms: from basic to clinical.Frontiers in cardiovascular medicine · 2024Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe role of N6-methyladenosine (m6A) modification in abdominal aortic aneurysm (AAA) has not been extensively studied. This study therefore aimed to investigate m6A RNA methylation and the expressions of the corresponding modulators in AAA.
methodsA comparative study between AAA tissue samples (n=32) and healthy aortas (n=12) was performed using m6A methylation quantification for messenger RNA (mRNA) m6A status, quantitative polymerase chain reaction (qPCR), and western blot for the expressions of m6A modulators and immunohistochemistry (IHC) to detect locations of the modulators in AAA tissues.
resultsThe m6A level significantly increased in AAA as compared to healthy aorta tissues. Among AAA patients, the high m6A level represented an even greater risk of AAA rupture as compared to non-ruptured AAA [odds ratio (OR), 1.370; 95% confidence interval (CI), 1.007-1.870]. The major N6-adenosine modulators, including YTHDF1, YTHDF3, FTO, and METTL14, are the main factors involved in aberrant m6A modification and the expression of both was significantly correlated to the proportion of m6A in total mRNA. Clinically, YTHDF3 represented an even greater risk of rupture (OR, 1.036; 95% CI, 1.001-1.072). Regarding the cellular location, METTL14 seemed to be associated with inflammatory infiltrates and neovascularization. Furthermore, a strong correlation was seen between FTO and aneurysmal smooth muscle cells (SMCs), YTHDF3, and macrophage infiltrate.
conclusionsWe were first to observe m6A modification in human AAA tissues. The results also reveal the important roles of m6A modulators, including YTHDF3, FTO, and METTL14, in the pathogenesis of human AAA and provide a new view on m6A modification in AAA. Our findings suggest a potential mechanism of epigenetic alterations in clinical AAA.
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