ArticleArthritis & rheumatology (Hoboken, N.J.)2022
Antiphospholipid Antibodies Increase Endometrial Stromal Cell Decidualization, Senescence, and Inflammation via Toll-like Receptor 4, Reactive Oxygen Species, and p38 MAPK Signaling.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- Preimplantation exposure to viral dsRNA impairs decidualization leading to altered placental development and fetal growth restriction.Reproduction & fertility · 2026Article
- Serum S100A8 as a potential biomarker for diagnosis of antiphospholipid syndrome and risk stratification among aPL carriers.Lupus science & medicine · 2026Article
- The role of TLR2/MyD88/NF-κB pathway-mediated macrophage M1 polarization in recurrent spontaneous abortion associated with antiphospholipid syndrome.Human cell · 2026Article
- Inhibition of FKBP5 alleviates obstetric antiphospholipid syndrome by regulating macrophage polarization.Scientific reports · 2025Article
- Regulation of cellular senescence in tumor progression and therapeutic targeting: mechanisms and pathways.Molecular cancer · 2025Review
- NK cells: shielding senescence homeostasis in the decidua during early pregnancy.Seminars in immunopathology · 2025Review
- Signaling pathways and advances in targeted therapy for adenomyosis.Frontiers in cell and developmental biology · 2025Review
- Multifunctional applications and research advances of low-molecular-weight heparin.Frontiers in pharmacology · 2025Review
- Predictors of Inflammation-Mediated Preterm Birth.Physiology (Bethesda, Md.) · 2025Review
- CDC42 deficiency leads to endometrial stromal cell senescence in recurrent implantation failure.Human reproduction (Oxford, England) · 2024Article
- Article
- TLR8-activating miR-146a-3p is an intermediate signal contributing to fetal membrane inflammation in response to bacterial LPS.Immunology · 2024Article
- Varied cellular abnormalities in thin vs. normal endometrium in recurrent implantation failure by single-cell transcriptomics.Reproductive biology and endocrinology : RB&E · 2024Article
- Hypoxia and the endometrium: An indispensable role for HIF-1α as therapeutic strategies.Redox biology · 2024Review
- Inhibition of Toll-like Receptors Alters Macrophage Cholesterol Efflux and Foam Cell Formation.International journal of molecular sciences · 2024Article
- Identifying the Anti-inflammatory Effects ofCombinatorial chemistry & high throughput screening · 2024Article
- The mTOR pathway in the antiphospholipid syndrome.Medical review (2021) · 2023Article
- The pathogenesis of obstetric APS: a 2023 update.Clinical immunology (Orlando, Fla.) · 2023Review
- Decidualization dampens toll-like receptor mediated inflammatory responses in human endometrial stromal cells by upregulating IκBα.Journal of reproductive immunology · 2023Article
- From Co-Infections to Autoimmune Disease via Hyperactivated Innate Immunity: COVID-19 Autoimmune Coagulopathies, Autoimmune Myocarditis and Multisystem Inflammatory Syndrome in Children.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
objectiveMiscarriage affects 1 in 7 pregnancies, and antiphospholipid autoantibodies (aPLs) are one of the biggest risk factors for recurrent pregnancy loss. While aPLs target the endometrial stroma, little is known about their impact. Endometrial stromal cells (EnSCs) undergo decidualization each menstrual cycle, priming the uterus to receive implanting embryos. Thus, appropriate decidualization and EnSC function is key for establishment of a successful pregnancy. This study was undertaken to explore the effects of aPL on EnSC decidualization, senescence, and inflammation.
methodsEnSCs under decidualizing conditions were exposed to aPL or control IgG alone or in the presence of either a Toll-like receptor 4 (TLR-4) antagonist, a p38 MAPK inhibitor, a reactive oxygen species (ROS) inhibitor, low molecular weight heparin (LMWH), or acetyl salicylic acid. Secretion of decidualization markers and inflammatory interleukin-8 were quantified by enzyme-linked immunosorbent assay, and senescence-associated β-galactosidase activity was evaluated. In a mouse model of decidualization, aPL or control IgG was administered, and uterine expression levels of decidualization and inflammatory markers were quantified by real-time quantitative polymerase chain reaction.
resultsAntiphospholipid antibodies increased human EnSC decidualization, senescence, and inflammation. This phenotype was recapitulated in the mouse model. The decidualization and inflammatory responses were partially mediated by TLR-4 and p38 MAPK, while the decidualization and senescence responses were ROS-dependent. LMWH, commonly used to treat aPL-positive women at risk of obstetric complications, reduced the ability of aPL to increase EnSC decidualization and inflammation.
conclusionThese findings shed new light on the pathogenesis of pregnancy complications in women with aPLs and underscore the benefit of heparin in preventing pregnancy loss in this high-risk population.
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