Therapeutically targeting mitochondrial redox signalling alleviates endothelial dysfunction in preeclampsia.

ABSTRACT: Aberrant placentation generating placental oxidative stress is proposed to play a critical role in the pathophysiology of preeclampsia. Unfortunately, therapeutic trials of antioxidants have been uniformly disappointing. There is provisional evidence implicating mitochondrial dysfunction as a source of oxidative stress in preeclampsia. Here we provide evidence that mitochondrial reactive oxygen species mediates endothelial dysfunction and establish that directly targeting mitochondrial scavenging may provide a protective role. Human umbilical vein endothelial cells exposed to 3% plasma from women with pregnancies complicated by preeclampsia resulted in a significant decrease in mitochondrial function with a subsequent significant increase in mitochondrial superoxide generation compared to

SUBMITTER: McCarthy C 

PROVIDER: S-EPMC5015016 | biostudies-literature | 2016 Sep

REPOSITORIES: biostudies-literature