The role of mitochondrial dysfunction in preeclampsia: Causative factor or collateral damage?

Alex N. Smith, Xi Wang, Daniel G. Thomas, Robert E. Tatum, George W. Booz, Mark W. Cunningham

Research output: Contribution to journalReview articlepeer-review

Abstract

Preeclampsia, new onset hypertension in pregnancy, affects -5%- 10% of the world's population. Preeclampsia is the leading cause of morbidity and mortality for both the mother and fetus. As of today, there is no cure for this disease except for delivery of the fetal-placental unit. The exact causation and onset of the disease are unknown. However, recent studies have shown a strong correlation between mitochondrial dysfunction and preeclampsia. Circulating mitochondrial DNA, elevated reactive oxygen species, angiotensin II type 1 receptor agonistic autoantibodies (AT1-AA), activated natural killer cells, and upregulated inflammatory responses all contribute to mitochondrial dysfunction and the pathophysiology of preeclampsia. This review summarizes the current literature of both experimental and clinical observations that support the hypothesis that mitochondrial dysfunction contributes to the pathophysiology of preeclampsia and may be a precursor to the disease onset. This review will also address the use of therapies to improve mitochondrial dysfunction in preeclampsia.

Original languageEnglish
Pages (from-to)442-452
Number of pages11
JournalAmerican journal of hypertension
Volume34
Issue number5
DOIs
StatePublished - 1 May 2021

Keywords

  • Blood pressure
  • Endothelial dysfunction
  • Hypertension
  • Inflammation
  • Innate immunity
  • Mitochondrial dysfunction
  • Natural killer cells
  • Oxidative stress
  • Preeclampsia

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