Aortic & peripheral vascular disease
NAT10 promotes vascular remodelling via mRNA ac4C acetylation
Authors' conclusion
This study reveals that NAT10 promotes vascular remodelling via mRNA ac4C acetylation, which may be a promising therapeutic target against vascular remodelling.
Study context
- Population
- Injured human and rodent arteries; Vascular smooth muscle cell (VSMCs)
Methodological detailsin-vitro and in-vivo vascular injury models, RNA sequence (RNA-seq), acRIP-seq and RIP-seq
- In-vitro and in-vivo vascular injury models
- RNA-seq, acRIP-seq and RIP-seq
Main finding
As reported in the abstract
- NAT10 and ac4C modifications upregulated in injured human and rodent arteries
- VSMC NAT10 deletion reduced post-injury neointima formation and VSMC phenotype switching
- NAT10, by ac4C modification, directly interacts with mRNAs incl. ITGB1 and Col1a2
- NAT10-mediated ac4C increased ITGB1 mRNA stability and downstream focal adhesion kinase (FAK) signaling, influencing VSMC proliferation and vascular remodelling
- Remodelin (NAT10 inhibitor) prevented neointima formation by suppressing VSMC proliferation, downregulating ITGB1 and deactivating FAK signaling
Original publication
NAT10 promotes vascular remodelling via mRNA ac4C acetylation. Eur Heart J. Published 25 October 2024. doi:10.
Summarised from the published abstract; every number is checked against it