Augmented expression of superoxide dismutase 2 mitigates progression and rupture of experimental abdominal aortic aneurysm.

ABSTRACT: Rationale: Oxidative stress is implicated in the pathogenesis and progression of abdominal aortic aneurysm (AAA). It is suggested that an excess in reactive oxygen species (ROS) over endogenous antioxidant activities can lead to endothelial and mitochondrial dysfunction, which promotes tissue inflammation, extracellular matrix degradation, and cellular apoptosis, all pathologic features characteristic of AAA. While elevated levels of ROS in human and experimental AAA appear well established, the contribution of endogenous antioxidant systems to aneurysm formation and progression remains controversial. We demonstrate that the antioxidant enzyme superoxide dismutase 2 (SOD2), the resident mitochondrial form of SODs that protects against mitochondrial damage, is relatively deficient in

SUBMITTER: Yan H 

PROVIDER: S-EPMC11980667 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature