Ncf1 knockout in smooth muscle cells exacerbates angiotensin II-induced aortic aneurysm and dissection by activating the STING pathway.

Hao LiuPeiwen YangShu Chen Shilin WangLang JiangXiaoyue XiaoSheng LeShanshan ChenXinzhong Chen Ping Ye Jiahong Xia

Published in: Cardiovascular research (2024)

Ncf1 deficiency in SMCs exacerbated Ang II-induced AAD by promoting NRF2 ubiquitination and degradation and activating the STING pathway. These data suggest that Ncf1 may be a potential therapeutic target for AAD treatment.

Keyphrases

angiotensin ii
high glucose
diabetic rats
vascular smooth muscle cells
angiotensin converting enzyme
aortic aneurysm
signaling pathway
oxidative stress
drug induced
electronic health record
endothelial cells