ArticleAntioxidants (Basel, Switzerland)2022
Mitochondria Targeted Antioxidant Significantly Alleviates Preeclampsia Caused by 11β-HSD2 Dysfunction via OPA1 and MtDNA Maintenance.
Article in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Oxidative Stress in Pathogenesis of Preeclampsia: Mechanistic and Clinical Insights.Antioxidants (Basel, Switzerland) · 2026Review
- Subtype specific immune-metabolic reprogramming in preeclampsia revealed by multiomics and serum biomarkers.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Article
- Altered Expression of Calpastatin by Hypoxia Regulates Trophoblast Cell Function through Mitochondria Associated Endoplasmic Reticulum Membranes.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Gut commensal bacterium Bacteroides vulgatus exacerbates helminth-induced cardiac fibrosis through succinate accumulation.PLoS pathogens · 2025Article
- Multiple analytical perspectives of mitochondrial genes in the context of preeclampsia: potential diagnostic markers.Frontiers in immunology · 2025Article
- Estrogen receptors in mitochondrial metabolism: age-related changes and implications for pregnancy complications.Aging advances · 2024Article
- Pregnancy Metabolic Adaptation and Changes in Placental Metabolism in Preeclampsia.Geburtshilfe und Frauenheilkunde · 2024Article
- Mitochondrial quality control alterations and placenta-related disorders.Frontiers in physiology · 2024Review
- [Research progress of optic atrophy 1-mediated mitochondrial dynamics in skeletal system diseases].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2023Review
- Mitochondrial ROS Accumulation Contributes to Maternal Hypertension and Impaired Remodeling of Spiral Artery but Not IUGR in a Rat PE Model Caused by Maternal Glucocorticoid Exposure.Antioxidants (Basel, Switzerland) · 2023Article
- Placental Mitochondrial Function and Dysfunction in Preeclampsia.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
We have previously demonstrated that placental 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) dysfunction contributes to PE pathogenesis. We sought to elucidate molecular mechanisms underlying 11β-HSD2 dysfunction-induced PE and to seek potential therapeutic targets using a 11β-HSD2 dysfunction-induced PE-like rat model as well as cultured extravillous trophoblasts (EVTs) since PE begins with impaired function of EVTs. In 11β-HSD2 dysfunction-induced PE-like rat model, we revealed that placental mitochondrial dysfunction occurred, which was associated with mitDNA instability and impaired mitochondrial dynamics, such as decreased optic atrophy 1 (OPA1) expression. MitoTEMPO treatment significantly alleviated the hallmark of PE-like features and improved mitDNA stability and mitochondrial dynamics in the placentas of rat PE-like model. In cultured human EVTs, we found that 11β-HSD2 dysfunction led to mitochondrial dysfunction and disrupted mtDNA stability. MitoTEMPO treatment improved impaired invasion and migration induced by 11β-HSD2 dysfunction in cultured EVTs. Further, we revealed that OPA1 was one of the key factors that mediated 11β-HSD2 dysfunction-induced excess ROS production, mitochondrial dysfunction and mtDNA reduction. Our data indicates that 11β-HSD2 dysfunction causes mitochondrial dysfunctions, which impairs trophoblast function and subsequently results in PE development. Our study immediately highlights that excess ROS is a potential therapeutic target for PE.
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