Targeting mitochondria-inflammation circle by renal denervation reduces atheroprone endothelial phenotypes and atherosclerosis.

ABSTRACT:

Objective

The disruption of mitochondrial redox homeostasis in endothelial cells (ECs) can cause chronic inflammation, a substantial contributor to the development of atherosclerosis. Chronic sympathetic hyperactivity can enhance oxidative stress to induce endothelial dysfunction. We determined if renal denervation (RDN), the strategy reducing sympathetic tone, can protect ECs by ameliorating mitochondrial reactive oxygen species (ROS)-induced inflammation to reduce atherosclerosis.

Methods and results

ApoE deficient (ApoE^-/-) mice were conducted RDN or sham operation before 20-week high-fat diet feeding. Atherosclerosis, EC phenotype and mitochondrial morphology were determined. In vitro, human arterial ECs were treated with norepinephrine to determine the mechan

SUBMITTER: Li Z 

PROVIDER: S-EPMC8498003 | biostudies-literature | 2021 Sep

REPOSITORIES: biostudies-literature