ArticleFrontiers in cellular neuroscience2019
Necrostatin-1 Ameliorates Peripheral Nerve Injury-Induced Neuropathic Pain by Inhibiting the RIP1/RIP3 Pathway.
Article in Frontiers in cellular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- RIPK1 inhibition reduces biliary injury and fibrosis in primary sclerosing cholangitis.Science advances · 2025Article
- The Effect of Pexidartinib on Neuropathic Pain via Influences on Microglia and Neuroinflammation in Mice.Anesthesia and analgesia · 2025Article
- MTOR Promotes Astrocyte Activation and Participates in Neuropathic Pain through an Upregulation of RIP3.Neurochemical research · 2025Article
- Construction of a Novel Necroptosis-Related Signature in Rat DRG for Neuropathic Pain.Journal of inflammation research · 2025Article
- Necrostatin-1: a promising compound for neurological disorders.Frontiers in cellular neuroscience · 2024Review
- Activation of the TNF-α-Necroptosis Pathway in Parvalbumin-Expressing Interneurons of the Anterior Cingulate Cortex Contributes to Neuropathic Pain.International journal of molecular sciences · 2023Article
- Ferroptosis: a new regulatory mechanism in neuropathic pain.Frontiers in aging neuroscience · 2023Review
- Necrostatin-1 decreases necroptosis and inflammatory markers after intraventricular hemorrhage in mice.Neural regeneration research · 2022Article
- Neuroimmune Mechanisms Underlying Neuropathic Pain: The Potential Role of TNF-α-Necroptosis Pathway.International journal of molecular sciences · 2022Review
- TNF-α-Mediated RIPK1 Pathway Participates in the Development of Trigeminal Neuropathic Pain in Rats.International journal of molecular sciences · 2022Article
- Electroacupuncture Alleviates Neuropathic Pain through Regulating miR-206-3p Targeting BDNF after CCI.Neural plasticity · 2022Article
- Advances in RIPK1 kinase inhibitors.Frontiers in pharmacology · 2022Review
- Iron Metabolism and Ferroptosis in Peripheral Nerve Injury.Oxidative medicine and cellular longevity · 2022Review
- Article
- RIP3-mediated necroptosis increases neuropathic pain via microglia activation: necrostatin-1 has therapeutic potential.FEBS open bio · 2021Article
- Preclinical Evidence for the Interplay between Oxidative Stress and RIP1-Dependent Cell Death in Neurodegeneration: State of the Art and Possible Therapeutic Implications.Antioxidants (Basel, Switzerland) · 2021Review
- Necroptosis in Macrophage Foam Cells Promotes Fat Graft Fibrosis in Mice.Frontiers in cell and developmental biology · 2021Article
- Mechanisms of neuroplasticity and brain degeneration: strategies for protection during the aging process.Neural regeneration research · 2021Article
- Compound Prunetin Induces Cell Death in Gastric Cancer Cell with Potent Anti-Proliferative Properties: In Vitro Assay, Molecular Docking, Dynamics, and ADMET Studies.Biomolecules · 2020Article
- Necrostatin-1 Alleviates Bleomycin-Induced Pulmonary Fibrosis and Extracellular Matrix Expression in Interstitial Pulmonary Fibrosis.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Necrostatin-1 is an inhibitor of necroptosis, a form of programmed cell death that has been reported to be involved in various neurological diseases. Presently, the role of necroptosis in neuropathic pain induced by peripheral nerve injury is still unclear. This study was focused on investigating the potential effects of necroptosis in the development and progression of neuropathic pain in a rat model and the possible neuroprotective effects of necrostatin-1 in neuropathic pain. The results indicated that the necroptosis-related proteins RIP1 and RIP3 significantly increased postoperation in the spinal cord in a neuropathic pain model and peaked 7 days postoperation, which was consistent with the time-dependent changes of hyperalgesia. Additionally, we found that peripheral nerve injury-related behavioral and biochemical changes were significantly reduced by necrostatin-1. In particular, hyperalgesia was attenuated, and the levels of RIP1 and RIP3 were decreased. Furthermore, the ultrastructure of necrotic cell death and neuroinflammation were alleviated by necrostatin-1. Collectively, these results suggest that necroptosis is an important mechanism of cell death in neuropathic pain induced by peripheral nerve injury and that necrostatin-1 may be a promising neuroprotective treatment for neuropathic pain.
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