ArticleThe American journal of pathology2019
AP39, a Modulator of Mitochondrial Bioenergetics, Reduces Antiangiogenic Response and Oxidative Stress in Hypoxia-Exposed Trophoblasts: Relevance for Preeclampsia Pathogenesis.
Article in The American journal of pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 74 citations in OpenAlex.
- HIF-1α mediated placental ischemic signaling in the development of early-onset preeclampsia.Redox biology · 2026Review
- Oxidative Stress in Pathogenesis of Preeclampsia: Mechanistic and Clinical Insights.Antioxidants (Basel, Switzerland) · 2026Review
- Mitochondria-Targeted Hydrogen Sulphide Delivery via an Adhesive Hydrogel Modulates Inflammation and Oxidative Stress in Diabetic Wounds.Gels (Basel, Switzerland) · 2026Article
- New Frontiers in the Pathophysiology of Hypertensive Pregnancy Disorders: A Systematic Review of Molecular Insights into Preeclampsia.Current issues in molecular biology · 2026Review
- Innovative mitochondria-based holistic 3PM approach to female health status: Facts and outlook.The EPMA journal · 2026Article
- Electrospun Polymer Fiber Mats for Persulfide Prodrug Delivery.Biomacromolecules · 2025Article
- Mitigating Oxidative Stress and Anti-Angiogenic State in an In Vitro Model of Preeclampsia by HY-12, an Organofluorine Hydrazone Antioxidant.Current issues in molecular biology · 2025Article
- Development of Diaryl Hydrazones for Alleviation of Mitochondrial Oxidative Stress in Preeclampsia.Journal of medicinal chemistry · 2025Article
- Integrated analysis of DNA methylation and transcriptome profiles to identify oxidative stress-related placenta-specific molecules for preeclampsia.The journal of obstetrics and gynaecology research · 2025Article
- Current Approaches and Innovations in Managing Preeclampsia: Highlighting Maternal Health Disparities.Journal of clinical medicine · 2025Review
- Article
- Solvent- and Catalyst-Free Environmentally Benign High Hydrostatic Pressure-Assisted Synthesis of Bioactive Hydrazones and the Evaluation of Their Stability Under Various Storage Conditions.Molecules (Basel, Switzerland) · 2024Article
- Normothermic ex vivo kidney perfusion preserves mitochondrial and graft function after warm ischemia and is further enhanced by AP39.Nature communications · 2024Article
- Diphenyl Diselenide Attenuates Mitochondrial Damage During Initial Hypoxia and Enhances Resistance to Recurrent Hypoxia.Neurotoxicity research · 2024Article
- The relationship between vitamin A and E levels and the severity of disease and oxidative stress injury in patients with preeclampsia.American journal of translational research · 2024Article
- A Novel Dual-Function Nitric Oxide Donor Therapy for Preeclampsia-A Proof-of-Principle Study in a Murine Model.Antioxidants (Basel, Switzerland) · 2023Article
- Article
- Nitroxide-HMP-Protects Human Trophoblast HTR-8/SVneo Cells from HAntioxidants (Basel, Switzerland) · 2023Article
- Mitochondria in endothelial cells angiogenesis and function: current understanding and future perspectives.Journal of translational medicine · 2023Review
- Effect of peroxiredoxin 1 on the regulation of trophoblast function by affecting autophagy and oxidative stress in preeclampsia.Journal of assisted reproduction and genetics · 2023Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Although the cause of preeclampsia, a pregnancy complication with significant maternal and neonatal morbidity, has not been fully characterized, placental ischemia attributable to impaired spiral artery remodeling and abnormal secretion of antiangiogenic factors are thought to be important in the pathogenesis of the disease. Placental ischemia could impair trophoblast mitochondrial function and energy production, leading to the release of reactive oxygen species (ROS). ROS have been shown to stabilize hypoxia-inducible factor (HIF)-1α, which, in turn, may induce transcription of antiangiogenic factors, soluble fms-like tyrosine kinase 1 (sFLT1), and soluble endoglin in trophoblasts. Herein, we tested whether the angiogenic imbalance and oxidative stress in the preeclamptic placenta may be prevented by improving mitochondrial function. First, to evaluate the cause-effect relationship between mitochondrial function and sFLT1 production, a human trophoblast primary cell culture model was established in which hypoxia induced mitochondrial ROS production and concurrent sFLT1 increase. Second, treatment with AP39, a novel mitochondria-targeted hydrogen sulfide donor, prevented ROS production, reduced HIF-1α protein levels, and diminished sFLT1 production. Finally, AP39, a modulator of mitochondrial bioenergetics enhanced cytochrome c oxidase activity, reversed oxidative stress and antiangiogenic response in hypoxic trophoblasts. These results suggest that placental hypoxia induces ROS production, HIF-1α stabilization, and sFLT1 up-regulation; these pathophysiological alterations can be attenuated by mitochondrial-targeted antioxidants.
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