ReviewCellular and molecular neurobiology2023
High-Mobility Group Box 1 in Spinal Cord Injury and Its Potential Role in Brain Functional Remodeling After Spinal Cord Injury.
Review in Cellular and molecular neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Interference with HMGB1 Inhibits Neuronal Ferroptosis Following Spinal Cord Injury through Targeting ACSL4.Neurochemical research · 2026Article
- Inflachromene Blocks Neuronal HMGB1 Translocation to Mitigate Hippocampal TLR4-NF-κB-Mediated Neuroinflammation and Depression-Like Behavior After Spinal Cord Injury.Molecular neurobiology · 2026Article
- Blood-spinal cord barrier disruption after spinal cord injury: a time-dependent mechanistic review.Frontiers in cellular neuroscience · 2026Review
- Inhibition of FOXD3 O-GlcNAc Modification Ameliorates Spinal Cord Injury by Promoting STUB1-Mediated Ubiquitination Degradation of HMGB1.Molecular neurobiology · 2025Article
- Involvement of circadian clock protein PER2 in controlling sleep deprivation induced HMGB1 up-regulation by targeting p300 in the cortex.Scientific reports · 2025Article
- Involvement of HMGB1-mediated ferroptosis in systemic diseases.Frontiers in cell and developmental biology · 2025Review
- Lentivirus-mediated RNA interference targeting HMGB1 modulates AQP1 to reduce pain induced by chronic compression of the dorsal root ganglia.Frontiers in pharmacology · 2024Article
- Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
High-mobility group box 1 (HMGB1) is a nonhistone nuclear protein, the functions of which depend on its subcellular location. It is actively or passively secreted into the blood and/or cerebrospinal fluid (CSF) and can be used as a prognostic indicator of disease. HMGB1 released into the bloodstream can cause pathological reactions in distant organs, and entry into the CSF can destroy the blood-brain barrier and aggravate brain injuries. HMGB1 expression has been reported to be increased in the tissues of spinal cord injury (SCI) patients and involved in the regulation of neuroinflammation, neuronal apoptosis, and ferroptosis. SCI can lead to brain changes, resulting in neuropathic pain, depression, and cognitive dysfunction, but the specific mechanism is unknown. It remains unclear whether HMGB1 plays an important role in brain functional remodeling after SCI. Damaged cells at the site of SCI passively release HMGB1, which travels to the brain via the blood, CSF, and/or axonal transport, destroys the blood-brain barrier, and causes pathological changes in the brain. This may explain the remodeling of brain function that occurs after SCI. In this minireview, we introduce the structure and function of HMGB1 and its mechanism of action in SCI. Clarifying the functions of HMGB1 may provide insight into the links between SCI and various brain regions.
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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.