Histone H3 dimethylation at lysine 79 is a key epigenetic mark uniquely induced by methyltransferase disruptor of telomeric silencing 1-like (DOT1L). We aimed to determine whether DOT1L modulates vascular smooth muscle cell (VSMC) phenotype and how it might affect atherosclerosis in vitro and in vivo, unravelling the related mechanism.

The epigenetic enzyme DOT1L orchestrates vascular smooth muscle cell-monocyte crosstalk and protects against atherosclerosis via the NF-κB pathway

Hall, Ignacio Fernando;Civilini, Efrem;Condorelli, Gianluigi;
2022-01-01

Abstract

Histone H3 dimethylation at lysine 79 is a key epigenetic mark uniquely induced by methyltransferase disruptor of telomeric silencing 1-like (DOT1L). We aimed to determine whether DOT1L modulates vascular smooth muscle cell (VSMC) phenotype and how it might affect atherosclerosis in vitro and in vivo, unravelling the related mechanism.
Dot1l
Atherosclerosis
Epigenetics
H3K79me2
Inflammation
Vascular smooth muscle cells
Humans
Mice
Animals
NF-kappa B
Histone-Lysine N-Methyltransferase
Monocytes
Myocytes, Smooth Muscle
Mice, Knockout
Gene Silencing
Cells, Cultured
Muscle, Smooth, Vascular
Atherosclerosis
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11699/70430
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus ND
  • ???jsp.display-item.citation.isi??? 6
social impact