TRAP1 drives smooth muscle cell senescence and promotes atherosclerosis via HDAC3-primed histone H4 lysine 12 lactylation.

Xuesong LiMinghong ChenXiang ChenXian HeXinyu LiHuiyuan WeiYongkang TanJiao MinTayyiba AzamMengdie XueYunjia ZhangMengdie DongQuanwen YinLongbin ZhengHong JiangDa HuoXin WangShaoliang ChenYong JiHongshan Chen

Published in: European heart journal (2024)

This study reveals a novel mechanism by which mitonuclear communication orchestrates gene expression in VSMC senescence and atherosclerosis. TRAP1-mediated metabolic reprogramming increases lactate-dependent H4K12la via HDAC3, promoting SASP expression and offering a new therapeutic direction for VSMC senescence and atherosclerosis.

Keyphrases

smooth muscle
gene expression
dna damage
endothelial cells
cardiovascular disease
stress induced
poor prognosis
histone deacetylase
dna methylation
single cell
cell therapy
type diabetes
stem cells
binding protein
long non coding rna
mesenchymal stem cells
amino acid