ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2010
Substance P antagonists as a therapeutic approach to improving outcome following traumatic brain injury.
Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
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.
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Who cites it
21 citing papers in PubMed, 55 citations in OpenAlex.
- Article
- Onabotulinumtoxin A for the Treatment of Post-Traumatic Headache: Is It Better than Anti-CGRP Antibodies?Toxins · 2024Review
- NK1 tachykinin receptor antagonist treatment reduces cerebral edema and intracranial pressure in an ovine model of ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- Substance P promotes the progression of bronchial asthma through activating the PI3K/AKT/NF-κB pathway mediated cellular inflammation and pyroptotic cell death in bronchial epithelial cells.Cell cycle (Georgetown, Tex.) · 2022Article
- A multi-staged neuropeptide response to traumatic brain injury.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2022Article
- Elevated Substance P Is a Risk Factor for Postoperative Delirium in Patients with Hip Fracture.BioMed research international · 2022Article
- Neurological heterotopic ossification: novel mechanisms, prognostic biomarkers and prophylactic therapies.Bone research · 2020Review
- Enhanced expressions of neurodegeneration-associated factors, UPS impairment, and excess Aβ accumulation in the hippocampus of mice with persistent cerebral toxocariasis.Parasites & vectors · 2017Article
- The role of substance P in epilepsy and seizure disorders.Oncotarget · 2017Review
- The Role of Substance P in Secondary Pathophysiology after Traumatic Brain Injury.Frontiers in neurology · 2017Review
- Neuropeptide substance P and the immune response.Cellular and molecular life sciences : CMLS · 2016Review
- Serum Levels of Substance P and Mortality in Patients with a Severe Acute Ischemic Stroke.International journal of molecular sciences · 2016Article
- Inflammation in acute CNS injury: a focus on the role of substance P.British journal of pharmacology · 2016Review
- Experimental diffuse brain injury results in regional alteration of gross vascular morphology independent of neuropathology.Brain injury · 2016Article
- Substance p regulates puberty onset and fertility in the female mouse.Endocrinology · 2015Article
- Serum substance P levels are associated with severity and mortality in patients with severe traumatic brain injury.Critical care (London, England) · 2015Observational
- Neuroprotection for traumatic brain injury.Handbook of clinical neurology · 2015Review
- Blocking neurogenic inflammation for the treatment of acute disorders of the central nervous system.International journal of inflammation · 2013Article
- Article
- Neuroprotection for traumatic brain injury: translational challenges and emerging therapeutic strategies.Trends in pharmacological sciences · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although a number of secondary injury factors are known to contribute to the development of morphological injury and functional deficits following traumatic brain injury, accumulating evidence has suggested that neuropeptides, and in particular substance P, may play a critical role. Substance P is released early following acute injury to the CNS as part of a neurogenic inflammatory response. In so doing, it facilitates an increase in the permeability of the blood-brain barrier and the development of vasogenic edema. At the cellular level, substance P has been shown to directly result in neuronal cell death; functionally, substance P has been implicated in learning and memory, mood and anxiety, stress mechanisms, emotion-processing, migraine, emesis, pain, and seizures, all of which may be adversely affected after brain injury. Inhibition of post-traumatic substance P activity, either by preventing release or by antagonism of the neurokinin-1 receptor, has consistently resulted in a profound decrease in development of edema and marked improvements in functional outcome. This review summarizes the current evidence supporting a role for substance P in acute brain injury.
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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.