ArticleGenes & diseases2026
Non-canonical role of "S6K1-SGK1" pathway in neuronal necroptosis following traumatic brain injury.
Article in Genes & diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Neuroprotective Mechanisms of Paeoniflorin in Parkinson's Models: Involvement of BDNF-Dependent PI3K/Akt and ERK/CREB Pathways.Current issues in molecular biology · 2026Article
- Thymosin Alpha-1 Provides Direct Neuroprotection by Engaging the Orexin Receptor HCRTR1 to Suppress Neuronal Necroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- [Geniposide inhibits retinal cell apoptosis induced by glaucoma through the Hspa1a pathway].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Article
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Authors and funding
11 authors.
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Abstract
Traumatic brain injury (TBI) is characterized by high rates of death and disability. Necroptosis is reported to be involved in neuronal death after TBI. However, additional molecules and related mechanisms underlying necroptosis, particularly during TBI, remain to be elucidated. mTOR and two of its three substrates (4EBP1 and ULK1) are involved in necroptosis. However, direct evidence linking necroptosis to S6K, another key substrate of mTORC1, has been lacking. In this study, we aimed to investigate the regulated role of "S6K1-glucocorticoid-inducible kinase-1 (SGK1)" pathway in neuronal necroptosis after TBI. We first showed that the "S6K1-SGK1" pathway was activated during neuronal necroptosis in TNF-α/Smac mimics/Z-VAD-FMK-induced necroptotic cell model and mouse TBI model. Then, inhibition of the "S6K1-SGK1" pathway could decrease necroptosis by regulating the MLKL activation. Next, a rescue assay indicated that S6K1 may regulate necroptosis through modulating SGK1 expression, while not through binding with SGK1. Finally, S6K1 inhibition alleviated neuronal necroptosis, neuro-inflammation, and functional damage via SGK1 in mice after TBI. Our results showed a non-canonical role of "S6K1-SGK1" pathway in neuronal necroptosis following TBI in mice, which will provide a potential therapeutic target for necroptosis treatment in TBI and other necroptosis-related disorders.
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