Deletion of METTL14, a key methylation regulator, attenuates vascular ageing
Authors' conclusion
This study hints at the role of METTL14/TLR4 signalling in the pathogenesis of vascular ageing
Study context
- Population
- Ageing mice, humans and senescent endothelial cells (HUVECs, human and mouse aortic endothelial cells)
- Comparison
- METTL14 knockdown/knockout vs overexpression in vascular ageing
Methodological detailsnatural ageing mouse model, D-galactose induced ageing mouse model, endothelial cell-specific METTL14 knockout mice
- Natural ageing mouse model
- D-galactose induced ageing mouse model
- Endothelial cell-specific METTL14 knockout mice
Main finding
As reported in the abstract
- METTL14 up-regulated in aortic endothelial cells of aged mice, aged humans and senescent endothelial cells
- Endothelium-specific METTL14 knockdown or knockout notably inhibited arterial stiffness, arterial remodelling and endothelial senescence; endothelium-specific overexpression had opposing effects
- METTL14 knockdown ameliorated cellular senescence, inflammatory responses and oxidative stress in senescent endothelial cells
- METTL14 facilitated m6A modification of TLR4 mRNA, enhancing its stability
- TLR4 knockdown reversed the detrimental effects of METTL14 on vascular ageing
- Vascular ageing, atherosclerosis and arteriosclerosis positively correlated with blood METTL14 and TLR4 elevations in humans
Original publication
Deletion of METTL14, a key methylation regulator, attenuates vascular ageing. Eur Heart J. Published 4 August 2025. doi:10.
Summarised from the published abstract; every number is checked against it