ReviewCytokine & growth factor reviews2014
Necrosis-dependent and independent signaling of the RIP kinases in inflammation.
Review in Cytokine & growth factor reviews, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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
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.
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Who cites it
50 citing papers in PubMed, 81 citations in OpenAlex.
- Tyrosine Kinase Receptors, Inhibition, and Potential Role in the Pharmacotherapy of Retinal Disorders.Ophthalmology and therapy · 2026Review
- Si-Miao-Yong-An decoction suppresses necroptosis by regulating the p53 pathway in myocardial ischemia/reperfusion injury.Scientific reports · 2025Article
- RIPK3 Contributes to Thyroid Hormone-Induced Photoreceptor Degeneration.International journal of molecular sciences · 2025Article
- Static magnetic field promotes the doxorubicin toxicity effects on osteosarcoma cells.Scientific reports · 2025Article
- RIPK3 and caspase-8 interpret cytokine signals to regulate ILC3 survival in the gut.Mucosal immunology · 2024Article
- RIPK3 signaling and its role in regulated cell death and diseases.Cell death discovery · 2024Review
- Key oncogenic signaling pathways affecting tumor-infiltrating lymphocytes infiltration in hepatocellular carcinoma: basic principles and recent advances.Frontiers in immunology · 2024Review
- Repositioning linifanib as a potent anti-necroptosis agent for sepsis.Cell death discovery · 2023Article
- Article
- Methodological advances in necroptosis research: from challenges to solutions.Journal of the National Cancer Center · 2022Article
- Necroptosis Blockade Potentiates the Neuroprotective Effect of Hypothermia in Neonatal Hypoxic-Ischemic Encephalopathy.Biomedicines · 2022Article
- Revisiting Regulated Cell Death Responses in Viral Infections.International journal of molecular sciences · 2022Review
- Direct T-2 Toxicity on Human Skin-Fibroblast Hs68 Cell Line-In Vitro Study.International journal of molecular sciences · 2022Article
- Opposite Effects of Apoptotic and Necroptotic Cellular Pathways on Rotavirus Replication.Journal of virology · 2022Article
- RIP3 blockade prevents immune-mediated hepatitis through a myeloid-derived suppressor cell dependent mechanism.International journal of biological sciences · 2022Article
- Role and mechanism of necrostin-1 in promoting oxidative stress response of macrophages in high glucose condition.Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2021Article
- Pleiotropic, non-cell death-associated effects of inhibitors of receptor-interacting protein kinase 1 in the heart.Molecular and cellular biochemistry · 2021Article
- Programmed cell death, redox imbalance, and cancer therapeutics.Apoptosis : an international journal on programmed cell death · 2021Review
- The expression of RIPK3 is associated with cell turnover of gastric mucosa in the mouse and human stomach.Journal of molecular histology · 2021Article
- Leaky Gut Driven by Dysbiosis Augments Activation and Accumulation of Liver MacrophagesFrontiers in immunology · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
It is now widely accepted that some forms of necrosis are controlled by a dedicated signaling pathway triggered by various cell surface and intracellular receptors. This regulated form of necrosis is mediated by the kinase activity of receptor-interacting protein kinase 1 (RIP1/RIPK1) and/or RIP3/RIPK3. A number of studies using the RIP1 kinase inhibitor Necrostatin-1 (Nec-1) and its derivatives, or RIP3-deficient mice demonstrated that RIP1 and RIP3 are involved in various infectious and sterile inflammatory diseases. As a consequence, these specific phenotypes were construed to depend on necrosis. However, emerging evidence indicates that the RIP1 kinase activity and RIP3 can also control apoptosis and inflammatory cytokine production independent of necrosis. Therefore, we may need to re-interpret conclusions drawn based on loss of RIP1 or RIP3 functions in in vivo models. We propose that studies of RIP1 and RIP3 in different inflammatory responses need to consider cell death-dependent and independent mechanisms of the RIP kinases.
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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.