ArticleThe journal of spinal cord medicine2015
Necroptosis, a novel type of programmed cell death, contributes to early neural cells damage after spinal cord injury in adult mice.
Article in The journal of spinal cord medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.
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Who cites it
67 citing papers in PubMed, 1 synthesis or guideline pooled it.
- A bibliometric analysis of the research hotspots and frontiers related to cell death in spinal cord injury.Frontiers in neurology · 2023Pooled it
- Safety, pharmacokinetics and target engagement of novel RIPK1 inhibitor SAR443060 (DNL747) for neurodegenerative disorders: Randomized, placebo-controlled, double-blind phase I/Ib studies in healthy subjects and patients.Clinical and translational science · 2022Trial
- Long non-coding RNAs: Emerging regulators of diverse programmed cell death pathways in neurons.Neural regeneration research · 2026Article
- Spinal cord extracellular matrix hydrogel enhances organoid maturation and functional regeneration after spinal cord injury.Materials today. Bio · 2026Article
- [Effect of composite graphene-protein hydrogels on neural regeneration after spinal cord injury in rats].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2026Article
- Roles for Exosomes from Various Cellular Sources in Spinal Cord Injury.Molecular neurobiology · 2025Review
- Traumatic spinal cord injury: a review of the current state of art and future directions - what do we know and where are we going?North American Spine Society journal · 2025Article
- Reanalysis of Published Histological Data Can Help to Characterize Neuronal Death After Spinal Cord Injury.International journal of molecular sciences · 2025Article
- Mechanisms of Traumatic Spinal Cord Injury AIS Grade Conversion.Neurotrauma reports · 2025Review
- Embryonic exposure to flubendiamide induces hepatotoxicity in domestic chicks by altering drug-metabolizing enzymes, antioxidant status, and liver function.Toxicology reports · 2024Article
- Critical Care of Spinal Cord Injury.Current neurology and neuroscience reports · 2024Review
- Evaluating Sex Steroid Hormone Neuroprotection in Spinal Cord Injury in Animal Models: Is It Promising in the Clinic?Biomedicines · 2024Review
- Targeted Therapy of Spinal Cord Injury: Inhibition of Apoptosis Is a Promising Therapeutic Strategy.Molecular neurobiology · 2024Review
- Advance in pediatric spinal cord injury.Pediatric discovery · 2024Review
- Astrocyte-Neuron Interactions in Spinal Cord Injury.Advances in neurobiology · 2024Review
- The Protein Acetylation after Traumatic Spinal Cord Injury: Mechanisms and Therapeutic Opportunities.International journal of medical sciences · 2024Review
- The role of purinergic receptors in neural repair and regeneration after spinal cord injury.Neural regeneration research · 2023Review
- Different Ways to Die: Cell Death Pathways and Their Association With Spinal Cord Injury.Neurospine · 2023Article
- Necrosulfonamide exerts neuroprotective effect by inhibiting necroptosis, neuroinflammation, and α-synuclein oligomerization in a subacute MPTP mouse model of Parkinson's disease.Scientific reports · 2023Article
- RIPK3 promoter hypermethylation in hepatocytes protects from bile acid-induced inflammation and necroptosis.Cell death & disease · 2023Article
7 more citing papers are in PubMed but not listed here.
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10 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundNecroptosis is an emerging programmed necrosis other than traditional necrosis and apoptosis. Until recently, there have not been studies that have investigated a relationship between necroptosis and pathogenesis of cell death after spinal cord injury (SCI).
objectiveTo investigate whether necroptosis takes part in the early pathophysiological processes of traumatic SCI in mice.
methodsFemale ICR mice were randomized equally into three groups: the sham, the vehicle-treated + SCI group, and the Nec-1-treated + SCI group. To induce SCI, the mice were subjected to a laminectomy at T9 and compression with a vascular clip. After mice were sacrificed 24 hours post-SCI, propidium iodide (PI)-positive cells were detected using in vivo PI labeling. Morphological analyses were performed by hematoxylin and eosin staining and Nissl staining. The samples were evaluated for apoptosis by the in situ TUNEL assay. The expression of caspase-3 was assessed by western blot. Locomotor behavior of hindlimb was evaluated by BMS (Basso mouse scale) score at 1, 3, 5, 7, and 14 days post-injury.
resultsCompared with dimethyl sulfoxide -treated mice, necrostatin-1-treated mice showed decreased PI-positive cells (P < 0.05), alleviated tissue damage, more surviving neuron at 24 hours after SCI (P < 0.05), and improved functional recovery from days 7 to 14 (P < 0.05). Necrostatin-1 did not reduce the expression of caspase-3 and the number of TUNEL-positive cells at 24 hours after SCI (P > 0.05).
conclusionsNecroptosis contributes to necroptotic cell death and influences functional outcome after SCI in adult mice. The inhibition of necroptosis by necrostatin-1 may have therapeutic potential for patients with SCI.
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