ReviewBehavioural neurology2018
The Pathogenesis of Necroptosis-Dependent Signaling Pathway in Cerebral Ischemic Disease.
Review in Behavioural neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Receptor-Interacting Protein Kinase 1 (RIPK1): A Potential Therapeutic Target in Ischemic Stroke.Molecular neurobiology · 2026Review
- Genetic Modification of Mesenchymal Stem Cell to Overexpress CXCR4 Enhances Treatment Efficacy for Brain Injury After Cardiopulmonary Resuscitation.CNS neuroscience & therapeutics · 2025Article
- A novel necroptosis related gene signature and regulatory network for overall survival prediction in lung adenocarcinoma.Scientific reports · 2023Article
- Agomelatine Exerts an Anti-inflammatory Effect by Inhibiting Microglial Activation Through TLR4/NLRP3 Pathway in pMCAO Rats.Neurotoxicity research · 2022Article
- Potential application of traditional Chinese medicine in cerebral ischemia-Focusing on ferroptosis.Frontiers in pharmacology · 2022Review
- Therapy Targets SARS-CoV-2 Infection-Induced Cell Death.Frontiers in immunology · 2022Review
- RNA modifications act as regulators of cell death.RNA biology · 2021Review
- The molecular mechanisms of MLKL-dependent and MLKL-independent necrosis.Journal of molecular cell biology · 2021Review
- Cell death-mediated cytokine release and its therapeutic implications.The Journal of experimental medicine · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Necroptosis is the best-described form of regulated necrosis at present, which is widely recognized as a component of caspase-independent cell death mediated by the concerted action of receptor-interacting protein kinase 1 (RIPK1) and receptor-interacting protein kinase 3 (RIPK3). Mixed-lineage kinase domain-like (MLKL) was phosphorylated by RIPK3 at the threonine 357 and serine 358 residues and then formed tetramers and translocated onto the plasma membrane, which destabilizes plasma membrane integrity leading to cell swelling and membrane rupture. Necroptosis is downstream of the tumor necrosis factor (TNF) receptor family, and also interaction with NOD-like receptor pyrin 3 (NLRP3) induced inflammasome activation. Multiple inhibitors of RIPK1 and MLKL have been developed to block the cascade of signal pathways for procedural necrosis and represent potential leads for drug development. In this review, we highlight recent progress in the study of roles for necroptosis in cerebral ischemic disease and discuss how these modifications delicately control necroptosis.
Indexed as
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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.