ArticleCell death & disease2025
SGK1 upregulation in GFAP
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
4 citing papers in PubMed.
- De Novo-Designed Peptide-Engineered Multimodal Platform for Post-Ischemic Stroke Tissue Repair.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Photothermal-Chemotherapeutic Microneedle Patch Coloaded with HMnOACS applied materials & interfaces · 2026Article
- SGK1 inhibition supports neuroprotection in spinal cord injury by suppressing oxidative stress and AIM2 activation via FoxO1 mediated mitophagy.Journal of neuroinflammation · 2026Article
- Visualizing Changes in Brain-Derived Neurotrophic Factor Expression in Living Mice Using the All-Engineered Bioluminescence Imaging System AkaBLI.Molecular neurobiology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Spinal cord injury (SCI) casts devastating and long-lasting impacts on the well-being of patients. Cognitive deficits and emotional disorders are common in individuals with SCI, yet the underlying mechanisms are not completely understood. Astrogliosis and glial scar formation occur during the subacute phase post-injury, playing complicated roles in remyelination and neurite regrowth. Therefore, we constructed a GFAP-IRES-Venus-AkaLuc knock-in mouse model for the corresponding studies. Surprisingly, complete spinal cord transection (SCT) surgery led to earlier and more prominent augmentation of bioluminescence in the brain than in the spinal cord. Bulk RNA sequencing revealed the activation of apoptotic signaling and the upregulation of serum and glucocorticoid-regulated kinase 1 (SGK1). The pattern of GFAP signals changed throughout the brain after SCT, as indicated by tissue clearing and immunostaining. Specifically, GFAP signals were intensified in the frontal association cortex (FrA), an encephalic region involved in associative learning and recognition memory processes. Further exploration unraveled that intensified GFAP signals in the FrA were attributed to apoptotic neurons with SGK1 upregulation, which was induced by sustained high glucocorticoid levels after SCT. The introduction of SGK1 silencing vectors confirmed that SGK upregulation in these FrA neurons exerted anti-apoptotic effects through NRF2/HO-1 signaling. In addition, SGK1 knockdown in FrA neurons aggravated the post-SCI depressive-like behaviors. Thus, ectopic SGK1 expression designated for limbic neurons could serve as a promising therapeutic target for the future development of treatments for spinal cord injuries.
Indexed as
Identifiers
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.