ArticleScience advances2023
Mitochondrial-targeted antioxidant attenuates preeclampsia-like phenotypes induced by syncytiotrophoblast-specific Gαq signaling.
Article in Science advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07229261 (MitoQ), which is not on this map. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
MitoQ (Mitoquinol Mesylate) to Ameliorate Vascular Function in Preeclampsia: a Novel Approach
Who cites it
13 citing papers in PubMed, 10 citations in OpenAlex.
- Oxidative stress in neurodegeneration: from a simple insult to a dynamic regulator.Redox report : communications in free radical research · 2026Review
- Evidence that S-phase kinase associated protein 2 (SKP2) is ubiquitinated and degraded via a Rho-related BTB domain containing 1 (RhoBTB1) and Cullin-3 mechanism in placenta.Physiological reports · 2026Article
- Spatially resolved fetal and maternal cell contributions to severe preeclampsia across gestation.Science advances · 2026Article
- Redox Imbalance in Gestational Diabetes Mellitus: Mechanistic Insights, Emerging Biomarkers, and Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- Biomimetic phycocyanin lipid-based nanoparticles ameliorate placental dysfunction and restore angiogenic balance in a pre-eclampsia model.Journal of nanobiotechnology · 2026Article
- Preeclampsia and environmental epigenomics: the emerging role of air pollution, gut microbiome, and maternal exposures in disease programming.Environmental epigenetics · 2026Review
- Genetic Association Between Rheumatoid Arthritis and Preeclampsia: A Bidirectional Mendelian Randomization and Bioinformatics Study.Maternal-fetal medicine (Wolters Kluwer Health, Inc.) · 2026Article
- Cuproptosis: a novel mechanism linking placental metabolic stress to trophoblast injury in preeclampsia.Frontiers in endocrinology · 2026Review
- The multifactorial role of HDAC9 at the maternal-fetal interface in the pathogenesis of preeclampsia.Clinical science (London, England : 1979) · 2025Review
- Localization and quantification of placentalPhysiological genomics · 2025Article
- Senescent Syncytiotrophoblast Secretion During Early Onset Preeclampsia.Hypertension (Dallas, Tex. : 1979) · 2025Article
- Intact NOX2 in T Cells Mediates Pregnancy-Induced Renal Damage in Dahl SS Rats.Hypertension (Dallas, Tex. : 1979) · 2024Article
- Placental and Renal Pathways Underlying Pre-Eclampsia.International journal of molecular sciences · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 2 institutions in 1 country.
Funding
Abstract
Syncytiotrophoblast stress is theorized to drive development of preeclampsia, but its molecular causes and consequences remain largely undefined. Multiple hormones implicated in preeclampsia signal via the Gαq cascade, leading to the hypothesis that excess Gαq signaling within the syncytiotrophoblast may contribute. First, we present data supporting increased Gαq signaling and antioxidant responses within villous and syncytiotrophoblast samples of human preeclamptic placenta. Second, Gαq was activated in mouse placenta using Cre-lox and DREADD methodologies. Syncytiotrophoblast-restricted Gαq activation caused hypertension, kidney damage, proteinuria, elevated circulating proinflammatory factors, decreased placental vascularization, diminished spiral artery diameter, and augmented responses to mitochondrial-derived superoxide. Administration of the mitochondrial-targeted antioxidant Mitoquinone attenuated maternal proteinuria, lowered circulating inflammatory and anti-angiogenic mediators, and maintained placental vascularization. These data demonstrate a causal relationship between syncytiotrophoblast stress and the development of preeclampsia and identify elevated Gαq signaling and mitochondrial reactive oxygen species as a cause of this stress.
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What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.