Journal
AMERICAN JOURNAL OF HYPERTENSION
Volume 34, Issue 5, Pages 442-452Publisher
OXFORD UNIV PRESS
DOI: 10.1093/ajh/hpab003
Keywords
blood pressure; endothelial dysfunction; hypertension; inflammation; innate immunity; mitochondrial dysfunction; natural killer cells; oxidative stress; preeclampsia
Categories
Funding
- American Heart Association [AHA 18CDA34110264]
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Preeclampsia, a new onset hypertension in pregnancy, affects 5%-10% of the world's population and is a leading cause of morbidity and mortality for both the mother and fetus. Recent studies suggest that mitochondrial dysfunction may contribute to the pathophysiology of preeclampsia, highlighting a potential avenue for therapeutic intervention.
Preeclampsia, new onset hypertension in pregnancy, affects similar to 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.
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