ArticlePloS one2021
Hypoxia-induced mitochondrial abnormalities in cells of the placenta.
Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 44 citations in OpenAlex.
- Understanding physiological adaptations of pregnancy to the chronic hypoxia of high altitude to inform obstetrical and neonatal care.Physiological reviews · 2026Review
- The Pathogenesis of Preeclampsia: Hypoxia and the Unfolded Protein Response.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Linking Oxidative Stress to Placental Dysfunction: The Key Role of Mitochondria in Trophoblast Function.Medical sciences (Basel, Switzerland) · 2026Review
- Shedding light on the function of autophagy in complicated pregnancies.Cell death & disease · 2026Review
- Research progress of quercetin in infection at the maternal-fetal interface.Frontiers in immunology · 2026Review
- The multifactorial role of HDAC9 at the maternal-fetal interface in the pathogenesis of preeclampsia.Clinical science (London, England : 1979) · 2025Review
- Normalization of trophoblast mTOR signaling rescues impaired function in primary human trophoblast cells isolated from pregnancies complicated by fetal growth restriction.Cell death discovery · 2025Article
- The uteroplacental circulation at high altitude: adaptation and maladaptation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- Placental mitochondria in high-altitude pregnancy: metabolic adaptations and a toolkit for respiratory assessment.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- Molecular and Biochemical Mechanisms of Cardiomyopathy Development Following Prenatal Hypoxia-Focus on the NO System.Antioxidants (Basel, Switzerland) · 2025Review
- Disparity Between Functional and Structural Recovery of Placental Mitochondria After Exposure to Hypoxia.International journal of molecular sciences · 2025Article
- Preeclampsia Treatment Aspirin/Clampsilin: Oxidative Stress, sFlt-1/PIGF Soluble Tyrosine Kinase 1, and Placental Growth Factor Monitoring.International journal of molecular sciences · 2024Article
- Placental Methylglyoxal in Preeclampsia: Vascular and Biomarker Implications.Hypertension (Dallas, Tex. : 1979) · 2024Article
- 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
- An integral role of mitochondrial function in the pathophysiology of preeclampsia.Molecular biology reports · 2024Review
- Effects of quercetin on immune regulation at the maternal-fetal interface.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2023Article
- Mitochondria in hypoxic pulmonary hypertension, roles and the potential targets.Frontiers in physiology · 2023Review
- Oxidative Regulation of Vascular CaAntioxidants (Basel, Switzerland) · 2022Review
- MicroRNA-210-mediated mtROS confer hypoxia-induced suppression of STOCs in ovine uterine arteries.British journal of pharmacology · 2022Article
- The Update of Fetal Growth Restriction Associated with Biomarkers.Maternal-fetal medicine (Wolters Kluwer Health, Inc.) · 2022Review
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionImpaired utero-placental perfusion is a well-known feature of early preeclampsia and is associated with placental hypoxia and oxidative stress. Although aberrations at the level of the mitochondrion have been implicated in PE pathophysiology, whether or not hypoxia-induced mitochondrial abnormalities contribute to placental oxidative stress is unknown.
methodsWe explored whether abnormalities in mitochondrial metabolism contribute to hypoxia-induced placental oxidative stress by using both healthy term placentae as well as a trophoblast cell line (BeWo cells) exposed to hypoxia. Furthermore, we explored the therapeutic potential of the antioxidants MitoQ and quercetin in preventing hypoxia-induced placental oxidative stress.
resultsBoth in placental explants as well as BeWo cells, hypoxia resulted in reductions in mitochondrial content, decreased abundance of key molecules involved in the electron transport chain and increased expression and activity of glycolytic enzymes. Furthermore, expression levels of key regulators of mitochondrial biogenesis were decreased while the abundance of constituents of the mitophagy, autophagy and mitochondrial fission machinery was increased in response to hypoxia. In addition, placental hypoxia was associated with increased oxidative stress, inflammation, and apoptosis. Moreover, experiments with MitoQ revealed that hypoxia-induced reactive oxygen species originated from the mitochondria in the trophoblasts. DISCUSSION: This study is the first to demonstrate that placental hypoxia is associated with mitochondrial-generated reactive oxygen species and significant alterations in the molecular pathways controlling mitochondrial content and function. Furthermore, our data indicate that targeting mitochondrial oxidative stress may have therapeutic benefit in the management of pathologies related to placental hypoxia.
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