The role of inflammation in CNS injury and disease
By Sian-Marie Lucas, N. Rothwell, R. Gibson. British Journal of Pharmacology, 2006
1,308 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology, Neurology
View Paper: https://www.semanticscholar.org/paper/d81cb8d6016387a548f2028aa2ce4aaa001107ee
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Immunology
- J. Tschopp
- Fabio Martinon
- P. Whitton
- M. Morganti‐Kossmann
- S. Doré
- Shizuo Akira
- T. Kanneganti
- Kate Schroder
In Molecular Biology
- J. Tschopp
- Fabio Martinon
- P. Whitton
- E. Candelario-Jalil
- M. Morganti‐Kossmann
- Andrzej Grzybowski
- M. Nita
- G. Burnstock
In Neurology
- P. Whitton
- M. Morganti‐Kossmann
- Andrzej Grzybowski
- M. Nita
- G. Burnstock
- S. Doré
- Elias K. Michaelis
- Guo-Yuan Yang
Citations in the corpus
- The Role of the Reactive Oxygen Species and Oxidative Stress in the Pathomechanism of the Age-Related Ocular Diseases and Other Pathologies of the Anterior and Posterior Eye Segments in Adults (2016, background): “Apoptotic processes are also activated by microglial cells, which release inflammatory mediators (cytokines, prostaglandins, and complement molecules) and reactive oxygen species [113].”
- Purinergic signalling and disorders of the central nervous system (2008, background): “The CNS can undergo all the typical changes induced by inflammation, activate endogenous inflammatory cells and generate inflammatory mediator”
- Involvement of pro- and anti-inflammatory cytokines and chemokines in the pathophysiology of traumatic brain injury (2011, background): “The inflammatory cascade activated after TBI is mediated by the release of pro- and anti-inflammatory cytokines, which are polypeptides, normally barely detectable in healthy tissue but rapidly upregulated in response to pathological or stressful challenges.(11,16) Besides their involvement in immun”
- Neuroinflammatory mechanisms of blood-brain barrier damage in ischemic stroke. (2019, background): “Following injury, microglia are activated and migrate to the damaged area where they can release proinflammatory cytokines such as IL-1 , TNF- , and IL-6, as well as other potential cytotoxic molecules, including NO, ROS, and prostaglandins (127).”
- IL‐1, IL‐18, and IL‐33 families of cytokines (2008, background): “Diseases of the central nervous system An extensive literature exists on the production of IL-1b by microglial and other cells in the brain, primarily in the hypothalamus (50, 51).”
- Inflammatory caspases and inflammasomes: master switches of inflammation (2007, background): “Similarly, IL-1b may be toxic for neurons and is involved in acute neurodegeneration and stroke.(29) Although many important biological effects of IL-1b are well described, key questions remain unresolved about the mechanism by which the production of this cytokine is regulated.”
- Inflammation as a causative factor in the aetiology of Parkinson's disease (2007, background): “prostaglandins and cytokines, which cause further disease progression (Arai et al., 2004, 2006; Lucas et al., 2006).”