ArticleCell death & disease2019
Pyroptosis is a critical inflammatory pathway in the placenta from early onset preeclampsia and in human trophoblasts exposed to hypoxia and endoplasmic reticulum stressors.
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 130 papers.
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Who cites it
130 citing papers in PubMed, 241 citations in OpenAlex.
- Late-onset preeclampsia is characterized by accelerated placental aging.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Pregnancy-related disorders: molecular mechanisms and management.Molecular biomedicine · 2026Review
- STOX1 Promotes Pyroptosis of Hypoxic Trophoblast Cells Via the Nrf2/Caspase-1 Axis.Molecular reproduction and development · 2026Article
- Endoplasmic Reticulum Stress-Induced Endothelial Cell Pyroptosis Contributes to Pulmonary Vascular Remodeling and Pulmonary Arterial Hypertension via IRE1α/Caspase-3/GSDME Pathway.Journal of the American Heart Association · 2026Article
- The Immunopathology of Preeclampsia.Biomedicines · 2026Review
- Kaempferol inhibited pyroptosis in preeclampsia by modulating the NLRP3 inflammasome through the STAT3-associated mitophagy pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- A new paradigm: 46 structural cell types function as environment-supporting innate immune cells, with endothelial and vascular smooth muscle cells as key prototypes.iNew medicine · 2026Article
- Stiripentol induces ER stress and pyroptosis in pancreatic cancer cells under metabolic stress by dysregulating SFAs/UFAs homeostasis.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Cell-Based and Cell-Free Non-Invasive Prenatal Analysis of Preeclampsia: An Updated Review of Liquid Biopsy.Biomedicines · 2026Review
- Revised Two-Stage Model of Preeclampsia Based on Autophagic Dysfunction: A Comprehensive Review.Biomolecules · 2026Review
- Caspase-3/GSDME-Mediated Trophoblast Pyroptosis and Reciprocal Macrophage Polarization Contribute to Inflammation in Early-Onset Preeclampsia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The β-hCG-TNF-α-T cell axis in threatened abortion: unraveling the pathogenic cascade from aberrant glycosylation to inflammatory demise.Frontiers in immunology · 2026Review
- Trophoblast invasion biology: from normal implantation to accreta spectrum and choriocarcinoma.Vascular biology (Bristol, England) · 2026Review
- Leveraging PANoptosis-associated genes for unraveling implication of decidualization deficiency in pre-eclampsia via transcriptome data and experiment validation.Frontiers in cell and developmental biology · 2026Article
- Regulated Cell Death at the Maternal-Fetal Interface in Preeclampsia: Apoptosis, Necroptosis, Pyroptosis, Ferroptosis, Autophagic Cell Death, and Cuproptosis - A Narrative Review.International journal of general medicine · 2026Review
- Endoplasmic reticulum stress-mediated programmed cell death in the tumor microenvironment.Cell death discovery · 2025Review
- Resveratrol Activates SIRT1 to Inhibit Trophoblast Pyroptosis in Preeclampsia.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- LAG3 as a Tumor Suppressor and Immune Regulator in Cervical Cancer: From Functional Validation to Therapeutic Strategy.Cancer medicine · 2025Article
- Therapeutic nanoparticle safety in pregnancy: Bridging knowledge gaps with environmental insights and a translational roadmap.Journal of controlled release : official journal of the Controlled Release Society · 2025Review
- Epicatechin inhibits inflammatory injury in preeclampsia extravillous trophoblasts.Reproduction (Cambridge, England) · 2025Article
70 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Systemic manifestation of preeclampsia (PE) is associated with circulating factors, including inflammatory cytokines and damage-associated molecular patterns (DAMPs), or alarmins. However, it is unclear whether the placenta directly contributes to the increased levels of these inflammatory triggers. Here, we demonstrate that pyroptosis, a unique inflammatory cell death pathway, occurs in the placenta predominantly from early onset PE, as evidenced by elevated levels of active caspase-1 and its substrate or cleaved products, gasdermin D (GSDMD), IL-1β, and IL-18. Using cellular models mimicking pathophysiological conditions (e.g., autophagy deficiency, hypoxia, and endoplasmic reticulum (ER) stress), we observed that pyroptosis could be induced in autophagy-deficient human trophoblasts treated with sera from PE patients as well as in primary human trophoblasts exposed to hypoxia. Exposure to hypoxia elicits excessive unfolded protein response (UPR) and ER stress and activation of the NOD-like receptor pyrin-containing 3 (NLRP3) inflammasome in primary human trophoblasts. Thioredoxin-interacting protein (TXNIP), a marker for hyperactivated UPR and a crucial signaling molecule linked to NLRP3 inflammasome activation, is significantly increased in hypoxia-treated trophoblasts. No evidence was observed for necroptosis-associated events. Importantly, these molecular events in hypoxia-treated human trophoblasts are significantly observed in placental tissue from women with early onset PE. Taken together, we propose that placental pyroptosis is a key event that induces the release of factors into maternal circulation that possibly contribute to severe sterile inflammation and early onset PE pathology.
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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.