ArticleJournal of pediatric surgery2018
Deficiency of receptor-interacting protein kinase 3 (RIPK3) attenuates inflammation and organ injury in neonatal sepsis.
Article in Journal of pediatric surgery, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Research trends and topics on sepsis immunosuppression: a bibliometric and visual analysis of global research from 2004 to 2024.Frontiers in medicine · 2025Pooled it
- Clinical impact of early-onset sepsis on outcomes of necrotizing enterocolitis: a retrospective case-control study.BMC pregnancy and childbirth · 2026Article
- Neutrophil in sepsis: functional aberration and regulated cell death.Frontiers in immunology · 2026Review
- The role of programmed cell death in organ dysfunction induced by opportunistic pathogens.Critical care (London, England) · 2025Review
- Crosstalk Between Cell Death and the cGAS-STING Pathway in Sepsis-Associated Acute Lung Injury.Journal of inflammation research · 2025Review
- Caspase-8 in inflammatory diseases: a potential therapeutic target.Cellular & molecular biology letters · 2024Review
- Circulating Markers of Necroptosis in Acute Pancreatitis.Digestive diseases and sciences · 2024Article
- Review
- RIPK3 promotes hantaviral replication by restricting JAK-STAT signaling without triggering necroptosis.Virologica Sinica · 2023Article
- Necroptosis: A Pathogenic Negotiator in Human Diseases.International journal of molecular sciences · 2022Review
- Interferon-γ Preferentially Promotes Necroptosis of Lung Epithelial Cells by Upregulating MLKL.Cells · 2022Article
- Dysregulation of neutrophil death in sepsis.Frontiers in immunology · 2022Review
- Signaling pathways and intervention therapies in sepsis.Signal transduction and targeted therapy · 2021Review
- The potential value of plasma receptor interacting protein 3 in neonates with culture-positive late-onset sepsis.BMC infectious diseases · 2021Article
- RIPK3 Facilitates Host Resistance to Oral Toxoplasma gondii Infection.Infection and immunity · 2021Article
- Clinical significance of miR-129-5p in patients with neonatal sepsis and its regulatory role in the LPS-induced inflammatory response.Bosnian journal of basic medical sciences · 2021Article
- M1 Macrophages Are More Susceptible to Necroptosis.Journal of cellular immunology · 2021Article
- Exploring Clinically-Relevant Experimental Models of Neonatal Shock and Necrotizing Enterocolitis.Shock (Augusta, Ga.) · 2020Review
- miR-425-5p improves inflammation and septic liver damage through negatively regulating the RIP1-mediated necroptosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Article
- Collateral damage: necroptosis in the development of lung injury.American journal of physiology. Lung cellular and molecular physiology · 2020Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
introductionSepsis is the third leading cause of morbidity and mortality in neonates. Sepsis in neonates is characterized as the systemic inflammation owing to infection within the first 28days after birth. The molecular mechanism causing the exaggerated inflammation phenotype in neonates has not been completely elucidated. Receptor interacting protein kinase 3 (RIPK3) is a protein identified as a mediator in programmed necrosis or necroptosis. We hypothesize that RIPK3 could be responsible for the inflammatory response in neonates and that deficiency in the RIPK3 protein attenuates inflammation and organ injury in neonatal sepsis.
methodsMale and female C57BL6 wild-type (WT) and RIPK3 knock-out (KO) newborn mice aged 5-7days (3-4g body weight) were injected intraperitoneally with 0.9mg/g cecal slurry (CS). At 10h after injection, the newborns were euthanized and blood, the lungs and gut tissues were collected.
resultsAt 10h after CS injection, serum cytokines IL-6 and IL-1β in the WT mice were increased by 511- and 43-fold whereas in KO mice, these levels were increased by 166-fold and 22-fold, respectively. Lung IL-1β in the WT mice increased by 7-fold after CS injection whereas only a 4-fold increase was seen in the KO mice. In the lungs of CS injected KO mice, the injury score, MIP-2 mRNA, myeloperoxidase (MPO) activity and TUNEL staining were significantly reduced by 76%, 70%, 26% and 74%, respectively compared to the CS WT mice. Gut TUNEL staining was also reduced by 80%.
conclusionThe deficiency in RIPK3 attenuated serum and lung cytokines, lung injury and neutrophil infiltration and lung and gut apoptosis. These data suggest that RIPK3, in part, is responsible for the systemic inflammatory response in neonatal sepsis.
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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.