ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2018
Soluble TNFα Signaling within the Spinal Cord Contributes to the Development of Autonomic Dysreflexia and Ensuing Vascular and Immune Dysfunction after Spinal Cord Injury.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- The Role of Tumor Necrosis Factor Following Spinal Cord Injury: A Systematic Review.Cellular and molecular neurobiology · 2023Pooled it
- Restoration of gamma-aminobutyric acid homeostasis: A novel approach to alleviating central nervous system injury-associated immunodepression syndrome.Neural regeneration research · 2026Article
- Frequency-Domain Analysis Links Autonomic Disruption to Renal Autoregulatory Failure after Spinal Cord Injury.bioRxiv : the preprint server for biology · 2026Article
- Integrative single-cell and bulk transcriptomic analyses identify a microglia-associated NAGLU signature linked to disulfidptosis-associated transcriptional patterns after spinal cord injury.Frontiers in immunology · 2026Article
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- NF-κB inhibition attenuates sympathetic hyperreflexia and concomitant development of autonomic dysreflexia and immune dysfunction after spinal cord injury.Communications biology · 2025Article
- Multifaceted Pathophysiology and Secondary Complications of Chronic Spinal Cord Injury: Focus on Pressure Injury.Journal of clinical medicine · 2025Review
- Evolving insights on the role of microglia in neuroinflammation, plasticity, and regeneration of the injured spinal cord.Frontiers in immunology · 2025Review
- Autonomic Dysreflexia in Spinal Cord Injury: Mechanisms and Prospective Therapeutic Targets.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024Review
- Mitigating sTNF/TNFR1 activation on VGluT2+ spinal cord interneurons improves immune function after mid-thoracic spinal cord injury.bioRxiv : the preprint server for biology · 2024Article
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- Spinal cord injury enhances lung inflammation and exacerbates immune response following exposure to LPS.Frontiers in immunology · 2024Article
- Unbiased multitissue transcriptomic analysis reveals complex neuroendocrine regulatory networks mediated by spinal cord injury-induced immunodeficiency.Journal of neuroinflammation · 2023Article
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- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Consequences of spinal cord injury on the sympathetic nervous system.Frontiers in cellular neuroscience · 2023Review
- Proinflammatory and Immunomodulatory Gene and Protein Expression Patterns in Spinal Cord and Spleen Following Acute and Chronic High Thoracic Injury.Journal of inflammation research · 2023Article
- Elevated levels of IgA and IgG2 in individuals with chronic spinal cord injury.The journal of spinal cord medicine · 2022Observational
- Maladaptation of renal hemodynamics contributes to kidney dysfunction resulting from thoracic spinal cord injury in mice.American journal of physiology. Renal physiology · 2022Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Cardiovascular disease and susceptibility to infection are leading causes of morbidity and mortality for individuals with spinal cord injury (SCI). A major contributor to these is autonomic dysreflexia (AD), an amplified reaction of the autonomic nervous system (hallmarked by severe hypertension) in response to sensory stimuli below the injury. Maladaptive plasticity of the spinal sympathetic reflex circuit below the SCI results in AD intensification over time. Mechanisms underlying this maladaptive plasticity are poorly understood, restricting the identification of treatments. Thus, no preventative treatments are currently available. Neuroinflammation has been implicated in other pathologies associated with hyperexcitable neural circuits. Specifically, the soluble form of TNFα (sTNFα) is known to play a role in neuroplasticity. We hypothesize that persistent expression of sTNFα in spinal cord underlies AD exacerbation. To test this, we intrathecally administered XPro1595, a biologic that renders sTNFα nonfunctional, after complete, high-level SCI in female rats. This dramatically attenuated the intensification of colorectal distension-induced and naturally occurring AD events. This improvement is mediated via decreased sprouting of nociceptive primary afferents and activation of the spinal sympathetic reflex circuit. We also examined peripheral vascular function using
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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.