ReviewInternational review of cell and molecular biology2017
The Inflammatory Signal Adaptor RIPK3: Functions Beyond Necroptosis.
Review in International review of cell and molecular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
60 citing papers in PubMed, 109 citations in OpenAlex.
- The dual role of RIPK family in IBD: from cell death to therapeutic targeting.Molecular medicine (Cambridge, Mass.) · 2026Review
- Oncogenic KRAS-driven type I interferon signalling primes pancreatic cancer for necroptosis.Nature communications · 2026Article
- The RIPK3 Inhibitor GSK872 Attenuates Inflammation and Necroptosis via Modulation of the JNK Signaling Pathway in LPS-Stimulated Microglia.Biomolecules & therapeutics · 2026Article
- RIPK3 Orchestrates Scar-Associated Macrophage Dysfunction to Drive Pulmonary Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Aberrant methylation limits antitumoral inflammation in lung adenocarcinoma by restricting RIPK3 expression.Science advances · 2026Article
- RIPK3 Protects Against Endothelial Activation and Vascular Permeability in a Mouse Model of Ischemia-Reperfusion Injury.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Microglial Necroptosis Mediated by RIPK3 Leads to Retinal Ganglion Cell Apoptosis Through the Release of FGF2 After Ischemia/Reperfusion.Journal of molecular neuroscience : MN · 2025Article
- Inactivation of PI3K-C2α deregulates cell death pathways and sensitizes to endotoxic shock.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- RIPK3 impacts antibody generation in an induced model of murine lupus through mechanisms other than necroptosis and antigen presentation.Frontiers in immunology · 2025Article
- Sodium formate induces development-dependent intestinal epithelial injury via necroptosis and apoptosis.Redox report : communications in free radical research · 2024Article
- Regulated Cell Death Pathways in Pathological Cardiac Hypertrophy.Reviews in cardiovascular medicine · 2024Review
- Circulating Markers of Necroptosis in Acute Pancreatitis.Digestive diseases and sciences · 2024Article
- RISING STARS: Evidence for established and emerging forms of β-cell death.The Journal of endocrinology · 2024Review
- RIPK3 signaling and its role in regulated cell death and diseases.Cell death discovery · 2024Review
- The mechanistic functional landscape of retinitis pigmentosa: a machine learning-driven approach to therapeutic target discovery.Journal of translational medicine · 2024Article
- Regulated cell death in chronic kidney disease: current evidence and future clinical perspectives.Frontiers in cell and developmental biology · 2024Review
- Inhibition of the RIP3/MLKL/TRPM7 necroptotic pathway ameliorates diabetes mellitus-induced erectile dysfunction by reducing cell death, fibrosis, and inflammation.Frontiers in pharmacology · 2024Article
- Macrophage RIPK3 triggers inflammation and cell death via the XBP1-Foxo1 axis in liver ischaemia-reperfusion injury.JHEP reports : innovation in hepatology · 2023Article
- Absence of Either Ripk3 or Mlkl Reduces Incidence of Hepatocellular Carcinoma Independent of Liver Fibrosis.Molecular cancer research : MCR · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Receptor interacting protein kinase 3 (RIPK3) is an essential serine/threonine kinase for necroptosis, a type of regulated necrosis. A variety of stimuli can cause RIPK3 activation through phosphorylation. Activated RIPK3 in turn phosphorylates and activates the downstream necroptosis executioner mixed lineage kinase domain-like (MLKL). Necroptosis is a highly inflammatory type of cell death because of the release of intracellular immunogenic contents from disrupted plasma membrane. Indeed, RIPK3-deficient mice exhibited reduced inflammation in many inflammatory disease models. These results have been interpreted as evidence that necroptosis is a key driver for RIPK3-induced inflammation. Interestingly, recent studies show that RIPK3 also regulates NF-κB, inflammasome activation, and kinase-independent apoptosis. These studies also reveal that these nonnecroptotic functions contribute significantly to disease pathogenesis. In this review, we summarize our current understanding of necroptotic and nonnecroptotic functions of RIPK3 and discuss how these effects contribute to RIPK3-mediated inflammation.
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What OpenQuestion holds
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.