ReviewJournal of advanced research2022
Role of necroptosis in traumatic brain and spinal cord injuries.
Review in Journal of advanced research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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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
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- A bibliometric analysis of the research hotspots and frontiers related to cell death in spinal cord injury.Frontiers in neurology · 2023Pooled it
- Post-Translational Modifications in Traumatic Brain Injury: Decoding the Proteomic Landscape and Molecular Mechanisms of Secondary Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Severity-dependent changes in hippocampal necroptosis markers and neuronal loss in a PTSD-like mouse model: potential involvement of nitric oxide signaling.Psychopharmacology · 2026Article
- Integrated Necroptosis Within Programmed Cell Death in Traumatic Brain Injury.Molecular neurobiology · 2026Review
- Non-canonical role of "S6K1-SGK1" pathway in neuronal necroptosis following traumatic brain injury.Genes & diseases · 2026Article
- Development of an HInternational journal of molecular sciences · 2026Article
- Study on the Function and Mechanism of Neutrophil Extracellular Traps in Regulating Necroptosis Following Traumatic Brain Injury.Brain and behavior · 2026Article
- PANoptosis and mitochondrial regulatory mechanisms in cerebral ischemia-reperfusion injury.Frontiers in physiology · 2026Review
- PANoptosis: a new perspective for targeting programmed cell death after spinal cord injury.Frontiers in immunology · 2026Review
- Neutrophil extracellular traps promote neuronal ferroptosis through STING-mediated AMPK dysregulation after traumatic brain injury.International journal of biological sciences · 2026Article
- Dynamic activation of lytic cell death-related programs identifies CD14 as a candidate hub gene associated with secondary injury after spinal cord injury.Frontiers in immunology · 2026Article
- Targeting microglial MyD88 reprograms injury-activated microglia and promotes spinal cord repair via TGF-β signaling and biomimetic nanodelivery.Theranostics · 2026Article
- Bioinformatics analysis and experimental validation reveal that heat HSP90AA1 enhances intestinal ischemia reperfusion induced necroptosis by inducing phosphorylated MLKL.Scientific reports · 2025Article
- RNA Interference and Its Key Targets for Spinal Cord Injury Therapy: What Is Known So Far?International journal of molecular sciences · 2025Review
- Inhibition of neuronal necroptosis via disruption of RIPK1-RIPK3 Interactions: The role of neural stem cell-derived exosomes in spinal cord injury recovery.Bioactive materials · 2025Article
- The Role of Autophagy in Long-term Effects of Spinal Cord Injury: Does Exosome Change the Autophagy Process and Vice Versa?Advanced pharmaceutical bulletin · 2025Review
- Traumatic Brian Injury (TBI) unraveled: molecular disruptions and therapeutic avenues.Inflammopharmacology · 2025Review
- From RIPK1 to Necroptosis: Pathogenic Mechanisms in Neurodegenerative Diseases.Neurochemical research · 2025Review
- Expression of RIPK-1 and S-100B in traumatic brain injury- exploring a forensic cases series.International journal of legal medicine · 2025Article
- Unraveling cell death mechanisms in traumatic brain injury: dynamic roles of ferroptosis and necroptosis.Molecular biology reports · 2025Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTraumatic brain injury (TBI) and spinal cord injury (SCI) are capable of causing severe sensory, motor and autonomic nervous system dysfunctions. However, effective treatments for TBI and SCI are still unavailable, mainly because the death of nerve cells is uncontrollable. Necroptosis is a type of programmed cell death and a critical mechanism in the process of neuronal cell death. However, the role of necroptosis has not been comprehensively defined in TBI and SCI. AIM OF REVIEW: This review aimed to summarize the role of necroptosis in central nervous system (CNS) trauma and its therapeutic implications and present important suggestions for researchers conducting in-depth research. KEY SCIENTIFIC CONCEPTS OF REVIEW: Necroptosis is orchestrated by a complex comprising the receptor-interacting protein kinase (RIPK)1, RIPK3 and mixed lineage kinase domain-like protein (MLKL) proteins. Mechanistically, RIPK1 and RIPK3 form a necrosome with MLKL. After MLKL dissociates from the necrosome, it translocates to the plasma membrane to induce pore formation in the membrane and then induces necroptosis. In this review, the necroptosis signalling pathway and the execution of necroptosis are briefly discussed. In addition, we focus on the existing information on the mechanism by which necroptosis participates in CNS trauma, particularly in the temporal pattern of RIPKs and in different cell types. Furthermore, we describe the association of miRNAs and necroptosis and the relationship between different types of CNS trauma cell death. Finally, this study highlights agents likely capable of curtailing such a type of cell death according to results optimization and CNS trauma and presents important suggestions for researchers conducting in-depth research.
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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.