[1][2] Astrogliosis changes the molecular expression and morphology of astrocytes, in response to infection for example, in severe cases causing glial scar formation that may inhibit axon regeneration.

They undergo a series of changes that may alter astrocyte activities through gain or loss of functions lending to neural protection and repair, glial scarring, and regulation of CNS inflammation.

[6][7] Reactive astrocytes defend against oxidative stress through glutathione production and have the responsibility of protecting CNS cells from NH4+ toxicity.

[3] They protect CNS cells and tissue through various methods,[3][8][9] such as uptake of potentially excitotoxic glutamate, adenosine release, and degradation of amyloid β peptides.

In its extreme form, reactive astrogliosis can lead to the appearance of newly proliferated astrocytes and scar formation in response to severe tissue damage or inflammation.

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.

[3] 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.

Upregulation of GFAP, which is induced by FGF, TGFB, and ciliary neurotrophic factor (CNTF), is a classic marker for reactive gliosis.

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.

In addition, AQP4, an astrocyte water channel, plays a crucial role in cytotoxic edema and aggravate outcome after stroke.

[16] Current studies are researching the possible benefits of inhibiting the inflammation caused by reactive gliosis in order to reduce its neurotoxic effects.

[2] Injection of ethidium bromide kills all CNS glia (oligodendrocytes and astrocytes), but leaves axons, blood vessels, and macrophages unaffected.