ReviewNeurochemical research2003
Response of chemokine antagonists to inflammation in injured spinal cord.
Review in Neurochemical research, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 20 citations in OpenAlex.
- In vitro and in vivo modulatory effects of fluoxetine on gene expression and antioxidant enzymes in CFA-induced chronic inflammatory model: drug repurposing for arthritis.Inflammopharmacology · 2024Article
- Article
- Extracellular matrix regulation of inflammation in the healthy and injured spinal cord.Experimental neurology · 2014Review
- A retinoic acid receptor beta agonist (CD2019) overcomes inhibition of axonal outgrowth via phosphoinositide 3-kinase signalling in the injured adult spinal cord.Neurobiology of disease · 2010Article
- Infiltrating blood-derived macrophages are vital cells playing an anti-inflammatory role in recovery from spinal cord injury in mice.PLoS medicine · 2009Article
- Mechanisms and implications of adaptive immune responses after traumatic spinal cord injury.Neuroscience · 2009Review
- Inflammation and its role in neuroprotection, axonal regeneration and functional recovery after spinal cord injury.Experimental neurology · 2008Review
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
Inflammation is a primary reaction to infection, allergic disorders, autoimmune diseases, and mechanical injury. The goal of an inflammatory response is to rapidly respond to noxious stimuli, such as trauma or pathogen, with a controlled amplification of cellular activation to eliminate, control, or wall off the triggering agent. Although the inflammatory response is necessary for resolution of the pathogenic event, by stander or collateral tissue damage is caused by the toxic nature of many of its by-products. It is characterized by the infiltration of leukocytes into the affected area. Chemokines and their receptors play an essential role as mediators of leukocyte infiltration. In most cases this response is so vigorous that its control, especially in the central nervous system, would inhibit recovery. The benefits of anti-inflammatory therapy based on interference with the chemokine system has been established in animal models and is being pursued with chemokine antibodies and receptor antagonists. Prolonged treatment with a broad-spectrum chemokine antagonist, vMIPII, has been shown to reduce the rate of infiltration of monocytes into injured rat spinal cord and promote survival.
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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.