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Prog Neurobiol. Apr;57(6) Reactive microgliosis. Streit WJ(1), Walter SA, Pennell NA. Author information: (1)Department of Neuroscience. Fibrous astrocytes become “hypertrophic” in early stages of reactive gliosis gliosis long astrocytic cell processes predominate with formation of a “glial scar”. attenuating reactive gliosis subsequent to arterial embolism = La asociación atorvastatina-meloxicam reduce el daño cerebral, atenuando la gliosis reactiva.

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Astrogliosis also known as astrocytosis or referred to as reactive astrocytosis is an abnormal increase in the number of astrocytes due to the destruction of nearby neurons from CNS traumainfectionischemiastrokeautoimmune responses, and neurodegenerative disease.

In healthy neural tissue, astrocytes play critical roles in energy provision, regulation of blood flow, homeostasis of extracellular fluid, homeostasis of ions and transmitters, regulation of synapse function, and synaptic remodeling. Reactive astrogliosis is a spectrum of changes in astrocytes that occur in response to all forms of central nervous system CNS injury reacfiva disease.

Changes due to reactive astrogliosis vary with the severity of the CNS insult along a graduated continuum of progressive alterations in molecular expression, progressive cellular hypertrophyproliferation and scar formation.

Insults to neurons in the central rdactiva system caused glioss infection, trauma, ischemia, stroke, autoimmune responses, or other neurodegenerative diseases may cause reactive astrocytes. When the astrogliosis is pathological itself, instead of a normal response to a pathological problem, it is referred to as astrocytopathy. Reactive astrocytes may benefit or harm surrounding neural and non-neural cells.

They undergo a series of changes that may alter astrocyte activities through gain or loss of functions lending to neural protection and repair, glial scarringand regulation of CNS inflammation. Proliferating reactive astrocytes are critical to scar formation and function to reduce the spread and persistence of inflammatory cellsto maintain the repair of the blood-brain barrier BBBto decrease tissue damage and lesion size, and to decrease neuronal loss and demyelination.

They have also been shown to reduce vasogenic edema after trauma, stroke, or obstructive hydrocephalus. Proliferating reactive scar-forming astrocytes are consistently found along borders between healthy tissues and pockets of damaged tissue and inflammatory cells.

This is usually found after a rapid, locally triggered inflammatory response to acute traumatic injury in the spinal cord and brain. In its extreme form, reactive astrogliosis can lead to the appearance of newly proliferated astrocytes and scar formation in response to severe tissue damage reactlva inflammation.

Mature astrocytes can re-enter the cell cycle and proliferate during scar formation.

Some proliferating reactive astrocytes can derive from NG2 progenitor cells in the local parenchyma from ependymal cell progenitors after injury or stroke. There are also multipotent progenitors in subependymal tissue that express glial fibrillary acidic protein GFAP and generate progeny cells that migrate towards sites of injury after trauma or stroke.


Reactive astrocytes are related to the normal function of astrocytes. Astrocytes are involved in the complex regulation of CNS inflammation that is likely to be context-dependent and regulated by multimodal extra- and intracellular signaling events. They have the capacity to make different types of molecules with either pro- or anti-inflammatory potential in response to different types of stimulation. Astrocytes interact extensively with microglia and play a key role in CNS inflammation.

Reactive astrocytes can then lead to abnormal function of astrocytes and affect their regulation and response rfactiva inflammation.

Pertaining to anti-inflammatory effects, reactive scar-forming astrocytes help reduce the spread of inflammatory cells during locally initiated inflammatory responses to traumatic injury or during peripherally-initiated adaptive immune responses. At early stages after insults, astrocytes not only activate inflammation, but also form potent cell migration barriers over time.

These barriers mark areas where intense inflammation is needed and restrict the spread of inflammatory cells and infectious agents to nearby healthy tissue. Inhibition of the migration of inflammatory cells and infectious agents have led to the accidental byproduct of axon regeneration inhibition, owing to the redundancy between migration cues across cell types. Changes resulting from astrogliosis are regulated in a context-specific manner by specific signaling events that have the potential to gliossis both the nature and degree of these changes.

Under different conditions of stimulation, astrocytes can produce intercellular effector molecules that alter the expression of molecules in cellular activities of cell structure, energy metabolism, intracellular signaling, and membrane transporters and pumps.

Molecular mediators are released by neuronsmicrogliaoligodendrocyte lineage cells, endothelialeukocytesand other astrocytes in the CNS tissue in response to insults ranging from subtle cellular perturbations to intense tissue injury. Few of the known signaling molecules and their effects are understood in the context of rectiva astrocytes responding to different degrees of insult.

Astrogliosis – Wikipedia

Paradoxically, an increase in GFAP production is also specific to the minimization of the lesion size and reduction in the risk for autoimmune encephalomyelitis and stroke. The presence of astrocyte glutamate transporters is associated with a reduced number of seizures and diminished neurodegeneration whereas the astrocyte gap junction protein Cx43 contributes to the neuroprotective effect of preconditioning to hypoxia.

In addition, AQP4an astrocyte water channel, plays a crucial role in cytotoxic edema and aggravate outcome after stroke. Loss or disturbance of functions normally performed by astrocytes or reactive astrocytes during the process of reactive astrogliosis has the potential to underlie neural dysfunction and pathology in various conditions including traumastrokemultiple sclerosisand others. Some of the examples are as reactlva Reactive astrocytes may also be reacgiva by specific reactica cascades to gain detrimental gliosos such as the following: Reactive astrocytes have the potential to promote neural toxicity via the generation cytotoxic molecules such as nitric oxide radicals and other reactive oxygen species[7] which may damage nearby neurons.


Reactive astrocytes may also promote secondary degeneration after CNS injury. Due to the destructive effects of astrogliosis, which include altered molecular expression, release of inflammatory factors, astrocyte proliferation and neuronal dysfunction, researchers are currently searching for new ways to treat astrogliosis and neurodegenerative diseases. Various studies have shown the role of astrocytes in diseases such as Alzheimer’samyotrophic lateral sclerosis ALSParkinson’sand Huntington’s.

Neurotrophins are currently being researched as possible drugs for neuronal protection, as they have been shown to restore neuronal function. For example, a few studies have used nerve growth factors to regain some cholinergic function in patients with Alzheimer’s. One specific drug candidate is BB14, which is a nerve growth factor-like peptide that acts as a TrkA agonist.

Further research of neurotrophins could potentially lead to the development of a highly selective, potent, and small neurotrophin that targets reactive gliosis to alleviate some neurodegenerative diseases.

TGFB is a regulatory molecule involved in proteoglycan production. This production is increased in the presence of bFGF or Interleukin 1. Injection of ethidium bromide kills all CNS glia oligodendrocytes and astrocytesbut leaves axons, blood vessels, and macrophages unaffected. After four days, CNS glia reinvade the area of injection and axonal regeneration is consequently inhibited.


Oligodendrocyte precursor cells and C6 glioma cells produce metalloproteinasewhich is shown to inactivate a type of inhibitory proteoglycan secreted by Schwann cells. Consequently, increased metalloproteinase in the environment around axons may facilitate axonal regeneration via degradation of inhibitory molecules due to increased proteolytic activity.

From Wikipedia, the free encyclopedia. Astrogliosis Reqctiva of reactive astrocytes after CNS injury. Journal of Neuroscience Research. Sofroniew, Astrogliosis, Advance, November 7,doi: Handbook of Experimental Pharmacology. Relevance to injury and recovery”. Retrieved from ” https: Articles which use infobox templates with no data rows.

Reactive microgliosis.

Views Read Edit View history. This page was last edited on 12 Februaryat By using this site, you agree to the Terms of Use and Privacy Policy. Formation of reactive astrocytes after CNS injury.

Anatomical terminology [ edit on Wikidata ].