The Role of Mitochondrial Dysfunction in Preeclampsia: Causative Factor or Collateral Damage?

Author:

Smith Alex N1,Wang Xi1,Thomas Daniel G1,Tatum Robert E1,Booz George W1,Cunningham Jr. Mark W1ORCID

Affiliation:

1. Department of Pharmacology and Toxicology, School of Medicine, University of Mississippi Medical Center, Jackson, MS USA

Abstract

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 is 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.

Publisher

Oxford University Press (OUP)

Subject

Internal Medicine

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