ArticleFrontiers in cardiovascular medicine2021
YTHDC2-Mediated circYTHDC2 N6-Methyladenosine Modification Promotes Vascular Smooth Muscle Cells Dysfunction Through Inhibiting Ten-Eleven Translocation 2.
Article in Frontiers in cardiovascular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 25 citations in OpenAlex.
- The mCells · 2026Review
- METTL3/YTHDC1 axis-mediated mMolecular medicine (Cambridge, Mass.) · 2026Article
- m6A modification of non‑coding RNA: Mechanisms, functions and potential values in human diseases (Review).International journal of molecular medicine · 2025Review
- Elevated CircYthdc2 expression is correlated with aggressive features and poor progression-free survival in hepatocellular carcinoma.BMC gastroenterology · 2025Article
- N6-methyladenosine methyltransferase Wilms tumor 1-associated protein impedes diabetic wound healing through epigenetically activating DNA methyltransferase 1.World journal of diabetes · 2025Article
- Exploring the methyl-verse: Dynamic interplay of epigenome and m6A epitranscriptome.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Novel Insight of N6-Methyladenosine in Cardiovascular System.Medicina (Kaunas, Lithuania) · 2025Review
- Epitranscriptome: A Novel Regulatory Layer during Atherosclerosis Progression.Current medicinal chemistry · 2025Review
- Circular RNAs in human diseases.MedComm · 2024Review
- The biological function of the N6-Methyladenosine reader YTHDC2 and its role in diseases.Journal of translational medicine · 2024Review
- The mFrontiers in endocrinology · 2024Review
- TET2 deficiency promotes anxiety and depression-like behaviors by activating NLRP3/IL-1β pathway in microglia of allergic rhinitis mice.Molecular medicine (Cambridge, Mass.) · 2023Article
- mActa biochimica et biophysica Sinica · 2023Review
- Integration of epigenetic regulatory mechanisms in heart failure.Basic research in cardiology · 2023Review
- The role of mFrontiers in endocrinology · 2023Review
- The Mechanism and Role ofJournal of cardiovascular development and disease · 2022Review
- The Role of NCells · 2022Review
- Circular RNAs in diabetes and its complications: Current knowledge and future prospects.Frontiers in genetics · 2022Review
- Metformin in aging and aging-related diseases: clinical applications and relevant mechanisms.Theranostics · 2022Review
- Correlation of TET-2 Levels with Disease Evaluation in AMI Patients.Contrast media & molecular imaging · 2022Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 2 diabetes condition mediated vascular smooth muscle cell (VSMCs) dysfunction. However, the mechanism of VSMCs dysfunction in diabetic patients needs further elucidation. VSMCs are an important component of the vascular wall, participate in the process of vascular remodeling, and play a vital role in the vascular complications of diabetes. Studies have found that circular RNAs (circRNAs) play a key regulatory role in the occurrence and development of VSMCs dysfunction. In this study, we stimulated VSMCs with high glucose and identified a new circular RNA, circYTHDC2, using circRNA chip analysis. circYTHDC2 was highly expressed in VSMCs treated with high glucose. Knockout of circYTHDC2 significantly inhibited the proliferation and migration of VSMCs. Metformin treatment significantly inhibited the expression of YTHDC2 and circYTHDC2. The upstream mechanism analysis revealed that the stability of circYTHDC2 was regulated by YTHDC2-mediated m6A modification. Furthermore, circYTHDC2 negatively regulates the expression of Ten-Eleven Translocation 2 (TET2) by targeting the unstable motif of TET2 3'UTR, thereby promoting dedifferentiated "synthetic type" transformation of VSMC. Taken together, these results suggest that the YTHDC2/circYTHDC2/TET2 pathway is an important target of metformin in preventing the progression of VSMCs dysfunction under high glucose.
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