Early onset of pathological polyploidization and cellular senescence in hepatocytes lacking RAD51 creates a pro-fibrotic and pro-tumorigenic inflammatory microenvironment.

Wenqing BuXue SunXiaotong XueShengmiao GengTingting YangJia ZhangYanan LiChao FengQiao LiuXiyu ZhangPeishan Li Zhaojian Liu Yufang Shi Changshun Shao

Published in: Hepatology (Baltimore, Md.) (2024)

Our results demonstrate a novel function of RAD51 in liver development, homeostasis, and tumorigenesis. The Rad51 -CKO mice represent a unique genetic model for premature liver senescence, fibrosis, and hepatocellular carcinogenesis.

Keyphrases

dna damage
early onset
dna repair
oxidative stress
late onset
anti inflammatory
endothelial cells
stem cells
genome wide
stress induced
idiopathic pulmonary fibrosis
type diabetes
copy number
liver injury
insulin resistance