Astrogliosis (also known as astrocytosis or referred to as reactive astrogliosis) is an abnormal increase in the number of astrocytes due to the destruction of nearby neurons from central nervous system (CNS) trauma, infection, ischemia, stroke, autoimmune responses or 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. 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. Causes Reactive astrogliosis is a spectrum of changes in astrocytes that occur in response to all forms of CNS injury and 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 hypertrophy, proliferation and scar formation. Insults to neurons in the central nervous system caused by infection, trauma, ischemia, stroke, recurring seizures, 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. Functions and effects 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 scarring, and regulation of CNS inflammation. Neural protection and repair Proliferating reactive astrocytes are critical to scar formation and function to reduce the spread and persistence of inflammatory cells, to maintain the repair of the blood–brain barrier (BBB), to decrease tissue damage and lesion size, and to decrease neuronal loss and demyelination. Reactive astrocytes defend against oxidative stress through glutathione production and have the responsibility of protecting CNS cells from NH4+ toxicity. They protect CNS cells and tissue through various methods, such as uptake of potentially excitotoxic glutamate, adenosine release, and degradation of amyloid β peptides. The repair of a disruption in the blood brain barrier is also facilitated by reactive astrocytes by their direct endfeet (characteristic structure of astrocytes) interaction with blood vessel walls that induce blood brain barrier properties. They have also been shown to reduce vasogenic edema after trauma, stroke, or obstructive hydrocephalus. Scar formation Proliferating reactive scar-forming astrocytes are consistently found along borders between healthy tissues and pockets of damaged