ArticlePlacenta2020
Palmitate induces apoptotic cell death and inflammasome activation in human placental macrophages.
Article in Placenta, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Programmed cell death in inflammation: interactions and holistic perspective.Cellular & molecular immunology · 2026Review
- Palmitate drives mitochondrial and ER stress through disruption of the CD73-Adenosine axis.Research square · 2026Article
- Folate receptor beta drives NLRP3 inflammasome activation and pyroptosis in macrophages independent of folate binding.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Comparison of cytokine responses to group BInfection and immunity · 2025Article
- NLRP3 Inflammasome-dependent Pathway is Involved in the Pathogenesis of Polycystic Ovary Syndrome.Reproductive sciences (Thousand Oaks, Calif.) · 2024Article
- Palmitate induces integrated stress response and lipoapoptosis in trophoblasts.Cell death & disease · 2024Article
- Biomarkers for Diagnosing and Treating Fetal Growth Restriction.Current medicinal chemistry · 2024Review
- Palmitate and group BFrontiers in immunology · 2024Article
- Placental DNA methylation changes in gestational diabetes mellitus.Epigenetics · 2022Article
- Preeclampsia and COVID-19: the Role of Inflammasome Activation.Current hypertension reports · 2022Review
- Immunometabolic adaptation and immune plasticity in pregnancy and the bi-directional effects of obesity.Clinical and experimental immunology · 2022Article
- Article
- Gestational Diabetes Mellitus and Maternal Immune Dysregulation: What We Know So Far.International journal of molecular sciences · 2021Review
- The Influence of Obesity and Associated Fatty Acids on Placental Inflammation.Clinical therapeutics · 2021Review
- NLRP3 inflammasome function and pyroptotic cell death in human placental Hofbauer cells.Journal of reproductive immunology · 2020Article
- Cellular immune responses in amniotic fluid of women with preterm prelabor rupture of membranes.Journal of perinatal medicine · 2020Article
- Macrophage Plasticity in Reproduction and Environmental Influences on Their Function.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
introductionThere is an increasing prevalence of non-communicable diseases worldwide. Metabolic diseases such as obesity and gestational diabetes mellitus (GDM) increasingly affect women during pregnancy, which can harm pregnancy outcomes and the long-term health and wellbeing of exposed offspring. Both obesity and GDM have been associated with proinflammatory effects within the placenta, the critical organ governing fetal development.
methodsThe purpose of these studies was to model, in vitro, the effects of metabolic stress (high levels of glucose, insulin and saturated lipids) on placental macrophage biology, since these cells are the primary innate immune phagocyte within the placenta with roles in governing maternofetal immune tolerance and antimicrobial host defense. Macrophages were isolated from the villous core of term, human placentae delivered through nonlaboring, elective Cesarean sections and exposed to combinations of elevated glucose (30 mM), insulin (10 nM) and the saturated lipid palmitic acid (palmitate, 0.4 mM).
resultsWe found that palmitate alone induced the activation of the nucleotide-binding oligomerization domain-like receptor (NLR) Family Pyrin Domain Containing 3 (NLRP3) inflammasome in placental macrophages, which was associated with increased interleukin 1 beta release and an increase in apoptotic cell death. Glucose and insulin neither provoked these effects nor augmented the impact of palmitate itself. DISCUSSION: Our findings confirm an impact of saturated fat on placental macrophage immune activation and could be relevant to the impact of metabolic stress in vivo.
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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.