Astrocyte activation and reactive gliosis
By M. Pekny, Michael Nilsson. Glia, 2005
1,598 citations recorded by the source corpus.
Subfields: Developmental Neuroscience, Molecular Biology, Neurology
View Paper: https://www.semanticscholar.org/paper/1ae7acbdc82b466aaee4c0f1082843d61abbcec6
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In Developmental Neuroscience
In Molecular Biology
In Neurology
Citations in the corpus
- Astrocytes: a central element in neurological diseases (2016, background): “ling cascades as reviewed elsewhere [109, 172, 174, 210, 213].”
- Glial fibrillary acidic protein (GFAP) and the astrocyte intermediate filament system in diseases of the central nervous system. (2015, background): “These results suggested that IF upregulation is an important component of reactive astrogliosis [2,24].”
- Astrocyte reactivity and reactive astrogliosis: costs and benefits. (2014, background): “This shows that IF upregulation is an important part of astrocyte activation and reactive astrogliosis, albeit not their proliferation in response to traumatic brain injury, and suggests a positive role for reactive astrocytes in the acute phase of neurotrauma (175, 176).”
- Genomic Analysis of Reactive Astrogliosis (2012, background): “The astrocytes’ abilities to help support neurons, regulate the blood– brain barrier, remodel the extracellular space, control immune cells, and control synapse formation and function may all be of great import in influencing how the brain fares during and following injury (Pekny and Nilsson, 2005; ”
- The role of glia in the spinal cord in neuropathic and inflammatory pain. (2015, background): “Following a change in their environment, such as that occurring in the spinal cord in models of chronic pain, these cells shift to a ‘reactive’ phenotype; astrocytes undergo hypertrophy and increase their expression of a number of cellular proteins including GFAP, S100β and vimentin, which are conse”
- Mechanism of Action of Oral Fingolimod (FTY720) in Multiple Sclerosis (2010, background): “Reactive astrocytes seem to play a beneficial role, especially in the acute stage after CNS injury but may later inhibit CNS regeneration.(112) Studies delivering S1P in vivo and in vitro have reported nervous system inflammatory responses that induce morphological changes in neural cells and astroc”
- Glial Lipid Droplets and ROS Induced by Mitochondrial Defects Promote Neurodegeneration (2015, neutral): “Similar morphological changes of glia have been reported under stress conditions (Boche et al., 2013; Pekny and Nilsson, 2005).”
- In vivo direct reprogramming of reactive glial cells into functional neurons after brain injury and in an Alzheimer’s disease model (2013, background): “Gliosis is a common pathological process after brain injury that involves the activation of glial cells to proliferate and become hypertrophic to occupy the injured brain areas (Pekny and Nilsson, 2005; Robel et al., 2011; Sofroniew and Vinters, 2010).”
- Neuroprotective effects of estradiol in hippocampal neurons and glia of middle age mice. (2007, background): “In this respect, cell proliferation in the granular layer of the DG of 18 month old female mice is 48% higher in a GFAP / Vimentin / background, suggesting that genetic attenuation of ageassociated reactive gliosis stimulates cell proliferation and neurogenesis (Larsson et al., 2004; Pekny and Nilss”
- The inflammatory response in stroke. (2007, background): “Following ischemia, brain astrocytes are activated resulting in increased glial fibrillary acidic protein (GFAP) expression and a so-called “reactive gliosis,” characterized by specific structural and functional changes (Pekny and Nilsson, 2005).”