Epigenetic and O-glycosylation regulation of p66Shc mitigates mitochondrial oxidative stress in aortic dissection.

ABSTRACT: Background: Aortic dissection (AD) is a life-threatening vascular emergency with limited effective pharmacological treatments. Recent studies have identified Src homology 2 domain-containing transforming protein C1 (p66Shc) as a crucial mediator of oxidative stress, apoptosis, and inflammation in aortic cells, thereby contributing to cellular dysfunction and vascular remodeling implicated in AD development and progression. Despite its established role in promoting vascular dysfunction and remodeling, the protective potential of targeting p66Shc in AD remains unclear. Methods: We quantified activated protein C (aPC) levels in clinical plasma samples from control subjects and AD patients using enzyme-linked immunosorbent assay (ELISA). To evaluate changes in p66Shc expression,

SUBMITTER: Zhang W 

PROVIDER: S-EPMC12906141 | biostudies-literature | 2026

REPOSITORIES: biostudies-literature