ReviewImmunology and cell biology2017
Mechanisms of RIPK3-induced inflammation.
Review in Immunology and cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 43 citations in OpenAlex.
- Single-cell time series analysis reveals the dynamics of HSPC response to inflammation.Life science alliance · 2024Article
- Inhibition of Urban Particulate Matter-Induced Airway Inflammation by RIPK3 through the Regulation of Tight Junction Protein Production.International journal of molecular sciences · 2023Article
- Inflammasome and Inflammatory Programmed Cell Death in Chromoblastomycosis.Mycopathologia · 2023Article
- A necroptosis-independent function of RIPK3 promotes immune dysfunction and prevents control of chronic LCMV infection.Cell death & disease · 2023Article
- Curcumin alleviates experimental colitis in mice by suppressing necroptosis of intestinal epithelial cells.Frontiers in pharmacology · 2023Article
- Inhibition of Pseudomonas aeruginosa LPS-Induced airway inflammation by RIPK3 in human airway.Journal of cellular and molecular medicine · 2022Article
- Article
- Mixed lineage kinase domain-like pseudokinase-mediated necroptosis aggravates periodontitis progression.Journal of molecular medicine (Berlin, Germany) · 2022Article
- Sepsis-induced AKI: From pathogenesis to therapeutic approaches.Frontiers in pharmacology · 2022Review
- Identification of the correlations between interleukin-27 (IL-27) and immune-inflammatory imbalance in preterm birth.Bioengineered · 2021Article
- RIPK3 signaling and its role in the pathogenesis of cancers.Cellular and molecular life sciences : CMLS · 2021Review
- Genetic inhibition of RIPK3 ameliorates functional outcome in controlled cortical impact independent of necroptosis.Cell death & disease · 2021Article
- Proteomic analysis of necroptotic extracellular vesicles.Cell death & disease · 2021Article
- RIP3 impedes transcription factor EB to suppress autophagic degradation in septic acute kidney injury.Cell death & disease · 2021Article
- RIPK3-mediated inflammation is a conserved β cell response to ER stress.Science advances · 2020Article
- RIPK3: A New Player in Renal Fibrosis.Frontiers in cell and developmental biology · 2020Review
- Flipping the dogma - phosphatidylserine in non-apoptotic cell death.Cell communication and signaling : CCS · 2019Review
- Sex-specific Tau methylation patterns and synaptic transcriptional alterations are associated with neural vulnerability during chronic neuroinflammation.Journal of autoimmunity · 2019Article
- RIPK3-deficient mice were not protected from nephrotoxic nephritis.BMC nephrology · 2018Article
- [Research progress on receptor interacting proteins in inflammation].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Receptor-interacting protein kinase 3 (RIP3/RIPK3) is a multifunctional regulator of cell death and inflammation. It controls signalling downstream of the tumor necrosis factor (TNF) receptor family, DNA-dependent activator of IFN-regulatory factors (DAI) and toll-like receptors (TLRs). Today, it is also widely recognized as a component of caspase-independent cell death known as necroptosis, and cytokine production via activation of the inflammasome. Its role in inflammasome activation, in particular, make the interpretation of its role in vivo more complex. In this review, we focus on divergent roles for RIPK3 in cell death and inflammation.
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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.