ArticleEuropean heart journal2025
Deletion of METTL14, a key methylation regulator, attenuates vascular ageing.
Article in European heart journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Deubiquitinases as Regulators and Therapeutic Targets in Vascular Diseases.International journal of molecular sciences · 2026Review
- The Role of NMedComm · 2026Review
- mRedox biology · 2026Review
- Nicotine promotes cardiac fibrosis by regulating miR-125b-5p maturation via HNRNPA2B1-mediated METTL14-dependent m⁶A methylation: therapeutic reversal by cinacalcet HCl.Journal of translational medicine · 2026Article
- Decoding Vascular Senescence: Cellular Insights and Therapeutic Strategies.International journal of biological sciences · 2026Review
- Endothelial senescence of the vertebral artery in the context of cervical degeneration: biomechanically driven remodeling of the hemodynamic environment.Frontiers in cell and developmental biology · 2026Review
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Authors and funding
20 authors.
Funding
Abstract
BACKGROUND AND
aimsVascular ageing often accompanies inflammation, contributing to the onset of local or systemic vascular diseases. Nevertheless, limited research focuses on pivotal factors triggering chronic vascular inflammation and associated pathological changes. This study aimed to investigate the role of methyltransferase-like protein 14 (METTL14) in inflammation in the pathogenesis of vascular ageing.
methodsThe natural ageing mouse model, D-galactose induced ageing mouse model, and endothelial cell-specific METTL14 knockout mice were generated. The roles of METTL14 in vascular ageing were investigated in human, mice, and various endothelial cells.
resultsUp-regulation of METTL14 was observed in the aortic endothelial cells of aged mice, aged humans, and senescent human umbilical vein endothelial cells, human aortic endothelial cells, and mice aortic endothelial cells. Endothelium-specific knockdown or knockout of METTL14 notably inhibited arterial stiffness, arterial remodelling, and endothelial senescence, whereas endothelium-specific overexpression of METTL14 yielded opposing effects. At the cellular level, METTL14 knockdown ameliorated cellular senescence, inflammatory responses, and oxidative stress in senescent endothelial cells. Mechanistically, METTL14 facilitated m6A modification of Toll-like receptor 4 (TLR4) mRNA, thereby enhancing its stability. Knockdown of TLR4 reversed the detrimental effects of METTL14 on vascular ageing. Importantly, vascular ageing, along with related atherosclerosis and arteriosclerosis, positively correlated with blood METTL14 and TLR4 elevations in humans.
conclusionsThis study hints at the role of METTL14/TLR4 signalling in the pathogenesis of vascular ageing, and METTL14 knockdown emerges as a potential therapeutic strategy for mitigating vascular ageing and associated vascular diseases.
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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 Socratic graph.