Dual functions of silibinin in attenuating aortic dissection via regulating iron homeostasis and endoplasmic reticulum stress against ferroptosis.

ABSTRACT: Aortic dissection (AD) poses a significant threat to cardiovascular health globally, yet its underlying mechanisms remain elusive. Smooth muscle cells death and phenotypic switching are critically important pathological processes in AD. Currently, no pharmacological therapies have proven effective in managing AD. This study aims to elucidate the involvement of ferroptosis in AD progression and explore ferroptosis inhibition as a potential therapeutic approach for AD management. Elevated expression of ferroptosis markers (HMOX1, ACSL4, and 4-HNE) was observed in AD patients and β-Aminopropionitrile (BAPN)-induced mice. In vivo administration of silibinin (SIL) attenuated aortic dilation, inflammation, mitochondrial injury, and ferroptosis. SIL treatment enhanced cell viability and mitochond

SUBMITTER: Qi Z 

PROVIDER: S-EPMC11655547 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature