ReviewCellular and molecular life sciences : CMLS2016
Necroptosis-independent signaling by the RIP kinases in inflammation.
Review in Cellular and molecular life sciences : CMLS, 2016. 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, 93 citations in OpenAlex.
- Review
- Caspase-8 silences cell death-independent constitutive immune activation driven by tonic TNF-α.EMBO reports · 2026Article
- Regulated necrosis at the crossroads of liver inflammation and cancer development.Nature reviews. Gastroenterology & hepatology · 2026Review
- RIP3 and MLKL regulate ER stress in alcohol-associated liver disease and pharmacological ER stress models: Insights beyond necroptosis.JHEP reports : innovation in hepatology · 2026Article
- Aberrant methylation limits antitumoral inflammation in lung adenocarcinoma by restricting RIPK3 expression.Science advances · 2026Article
- ZBP1 Mediates Renal Tubular Injury in Diabetic Nephropathy Through RIPK3-mediated Necroptosis.Inflammation · 2026Article
- Initiation of Tertiary Lymphoid Structures for Cancer Immunotherapy.Research (Washington, D.C.) · 2026Review
- HIV-Induced Apoptosis: Host Defense and Viral Strategy.Biology · 2025Review
- RIP3 and MLKL regulate Hepatic ER stress in alcohol-associated liver disease and pharmacological ER stress models: insights beyond necroptosis.bioRxiv : the preprint server for biology · 2025Article
- Suppression of necroptosis-driven cell death and inflammation in hypoxic neuroblastoma (SH-SY5Y) cells by necrostatin-1.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Astrocytic RIPK3 exerts protective anti-inflammatory activity in mice with viral encephalitis by transcriptional induction of serpins.Science signaling · 2025Article
- Phosphoglycerate Mutase 5 Is Important Mediator for Instigating Arterial Lipid Accumulation and Aggravating Atherosclerosis.JACC. Basic to translational science · 2025Article
- RIPK1 signaling pathways: implications for autoimmune and neuroinflammatory diseases.Frontiers in immunology · 2025Review
- Targeting TNFR1-driven necroptosis in breast cancer.EXCLI journal · 2025Review
- Genomic and Transcriptional Analysis of the Necroptosis Pathway Elements RIPK and MLKL in Sea Cucumber,Genes · 2024Article
- RIPK1 inhibition mitigates neuroinflammation and rescues depressive-like behaviors in a mouse model of LPS-induced depression.Cell communication and signaling : CCS · 2024Article
- RIPK3 promotes islet amyloid-induced β-cell loss and glucose intolerance in a humanized mouse model of type 2 diabetes.Molecular metabolism · 2024Article
- CSFV restricts necroptosis to sustain infection by inducing autophagy/mitophagy-targeted degradation of RIPK3.Microbiology spectrum · 2024Article
- Caspase-8 inhibition improves the outcome of bacterial infections in mice by promoting neutrophil activation.Cell reports. Medicine · 2023Article
- ZBP1 Protects Against mtDNA-Induced Myocardial Inflammation in Failing Hearts.Circulation research · 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
Recent advances have identified a signaling cascade involving receptor interacting protein kinase 1 (RIPK1), RIPK3 and the pseudokinase mixed lineage kinase domain-like (MLKL) that is crucial for induction of necroptosis, a non-apoptotic form of cell death. RIPK1-RIPK3-MLKL-mediated necroptosis has been attributed to cause many inflammatory diseases through the release of cellular damage-associated molecular patterns (DAMPs). In addition to necroptosis, emerging evidence suggests that these necroptosis signal adaptors can also facilitate inflammation independent of cell death. In particular, the RIP kinases can drive NF-κB and inflammasome activation independent of cell death. In this review, we will discuss recent discoveries that led to this realization and present arguments why cell death-independent signaling by the RIP kinases may have a more important role in inflammation than necroptosis.
Indexed as
Identifiers
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.