ArticleCell death & disease2019
The fine-tuning of endoplasmic reticulum stress response and autophagy activation during trophoblast syncytialization.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Review
- Trophoblast aging driven by IL33 deficiency elevates recurrent pregnancy loss risk through SNAP29 lactylation-mediated autophagy impairment.Autophagy · 2026Article
- Metabolic imprinting in trophoblast barrier dysfunction: the role of glucolipotoxicity, endoplasmic reticulum stress, and amino acid transport imbalance.Journal of assisted reproduction and genetics · 2026Review
- BAP1 dysregulation impairs trophoblast differentiation and contributes to placental dysfunction in preeclampsia.Cell death & disease · 2026Article
- Shedding light on the function of autophagy in complicated pregnancies.Cell death & disease · 2026Review
- Review
- Trophoblast adaptation to hypoxia: balance and dysfunction.Cell communication and signaling : CCS · 2025Review
- Autophagy in PE: Dispute, Role and Potential Target.Cell proliferation · 2025Review
- Role of ferroptosis-related GPX4 signaling in the fusion of human trophoblast cells.Scientific reports · 2025Article
- Single-nucleus transcriptional profiling of the placenta reveals the syncytiotrophoblast stress response to COVID-19.American journal of obstetrics and gynecology · 2025Article
- Development of apical out trophoblast stem cell derived organoids to model early human pregnancy.iScience · 2025Article
- Artificial plasticenta: how polystyrene nanoplastics affectFrontiers in cell and developmental biology · 2025Article
- Autophagy in reproduction and pregnancy-associated diseases.iScience · 2024Review
- The regulated cell death at the maternal-fetal interface: beneficial or detrimental?Cell death discovery · 2024Review
- A stress paradox: the dual role of the unfolded protein response in the placenta.Frontiers in endocrinology · 2024Review
- The Role of Autophagy in the Female Reproduction System: For Beginners to Experts in This Field.Biology · 2023Review
- Association of maternal thyroid peroxidase antibody during pregnancy with placental morphology and inflammatory and oxidative stress responses.Frontiers in endocrinology · 2023Article
- Regulators involved in trophoblast syncytialization in the placenta of intrauterine growth restriction.Frontiers in endocrinology · 2023Review
- Linking unfolded protein response to ovarian cancer cell fusion.BMC cancer · 2022Article
- Expression of ABC transporters during syncytialization in preeclampsia.Pregnancy hypertension · 2022Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The syncytiotrophoblast (STB) is a multinuclear layer forming the outer surface of the fetal part of the placenta deriving from villous cytotrophoblastic cell (vCTB) fusion and differentiation. This syncytialization process is characterized by morphological and biochemical alterations of the trophoblast, which probably require removal of pre-existing structures and proteins to maintain cell homeostasis and survival. Interestingly, autophagy, which allows degradation and recycling of cellular components, was shown to be activated in syncytiotrophoblast. Here we examined the involvement of endoplasmic reticulum stress (ERS) response in autophagy activation during vCTB syncytialization. We first demonstrated the activation of ERS response and autophagy during the time course of trophoblastic cell fusion and differentiation. Alteration of autophagy activation in vCTB by chemical treatments or Beclin-1 expression modulation leads to a decrease in trophoblastic syncytialization. Furthermore, ERS response inhibition by chemical treatment or siRNA strategy leads to a default in syncytialization, associated with alteration of autophagy markers and cell survival. From these data, we suggest that ERS response, by fine regulation of autophagy activation, may serve as an adaptive mechanism to promote cell survival during trophoblastic syncytialization.
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