ArticlePloS one2020
Reactive oxygen species from mitochondria impacts trophoblast fusion and the production of endocrine hormones by syncytiotrophoblasts.
Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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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.
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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.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Analysis of the evolution of placental oxidative stress research from a bibliometric perspective.Frontiers in pharmacology · 2024Pooled it
- Trophoblast metabolic reprogramming triggers adverse pregnancy outcomes during DENV-2 infection in mice.Journal of virology · 2026Article
- Phytochemical, antioxidant, and antimicrobial properties ofJournal of food science and technology · 2026Article
- Cannabis smoke extract disrupts trophoblast differentiation and causes mitochondrial dysfunction beyond the effects of Δ9-THC alone.Scientific reports · 2026Article
- Trophoblast Function in Preeclampsia: Decoding the Mechanistic Roles of Coding and Non-Coding Genes.International journal of molecular sciences · 2025Review
- Placental mitochondrial calcium uniporter modulates offspring susceptibility to metabolic dysfunction.Molecular metabolism · 2025Article
- Bovine Endometrium Drives and Responds to Divergence of In Vitro Produced Conceptus Biochemistry.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Gestational trophoblastic disease: understanding the molecular mechanisms of placental tumours.Disease models & mechanisms · 2025Review
- Oxidative stress induces release of mitochondrial DNA into the extracellular space in human placental villous trophoblast BeWo cells.American journal of physiology. Cell physiology · 2024Article
- The GPI-anchor biosynthesis pathway is critical for syncytiotrophoblast differentiation and placental development.Cellular and molecular life sciences : CMLS · 2024Article
- Maternal supplementation with n-3 fatty acids affects placental lipid metabolism, inflammation, oxidative stress, the endocannabinoid system, and the neonate cytokine concentrations in dairy cows.Journal of animal science and biotechnology · 2024Article
- Article
- Unraveling the nexus of age, epilepsy, and mitochondria: exploring the dynamics of cellular energy and excitability.Frontiers in pharmacology · 2024Review
- Trained innate immunity as a potential link between preeclampsia and future cardiovascular disease.Frontiers in endocrinology · 2024Review
- Beta-Carotene Supplementation for Sows: Reproductive Parameters and Productive Performance of Piglets.Animals : an open access journal from MDPI · 2023Article
- Mitochondrial-targeted antioxidant attenuates preeclampsia-like phenotypes induced by syncytiotrophoblast-specific Gαq signaling.Science advances · 2023Article
- Mitochondrial Dysfunction as a Signaling Target for Therapeutic Intervention in Major Neurodegenerative Disease.Neurotoxicity research · 2023Review
- The Implications of Cannabinoid-Induced Metabolic Dysregulation for Cellular Differentiation and Growth.International journal of molecular sciences · 2023Review
- Micro-RNAs in Human Placenta: Tiny Molecules, Immense Power.Molecules (Basel, Switzerland) · 2022Review
- How trophoblasts fuse: an in-depth look into placental syncytiotrophoblast formation.Cellular and molecular life sciences : CMLS · 2022Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The placenta, a tissue that is metabolically active and rich in mitochondria, forms a critical interface between the mother and developing fetus. Oxidative stress within this tissue, derived from the dysregulation of reactive oxygen species (ROS), has been linked to a number of adverse fetal outcomes. While such outcomes have been associated with mitochondrial dysfunction, the causal role of mitochondrial dysfunction and mitochondrially generated ROS in altering the process of placentation remains unclear. In this study, mitochondrial complex I activity was attenuated using 10 nM rotenone to induce cellular oxidative stress by increasing mitochondrial ROS production in the BeWo choriocarcinoma cell line. Increased mitochondrial ROS resulted in a significant decrease in the transcripts which encode for proteins associated with fusion (GCM1, ERVW-1, and ERVFRD-1) resulting in a 5-fold decrease in the percentage of BeWo fusion. This outcome was associated with increased indicators of mitochondrial fragmentation, as determined by decreased expression of MFN2 and OPA1 along with an increase in a marker of mitochondrial fission (DRP1). Importantly, increased mitochondrial ROS also resulted in a 5.0-fold reduction of human placental lactogen (PL) and a 4.4-fold reduction of insulin like growth factor 2 (IGF2) transcripts; hormones which play an important role in regulating fetal growth. The pre-treatment of rotenone-exposed cells with 5 mM N-acetyl cysteine (NAC) resulted in the prevention of these ROS mediated changes in BeWo function and supports a central role for mitochondrial ROS signaling in the maintenance and function of the materno-fetal interface.
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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 OpenQuestion graph.