Gliosis

Gliosis is a nonspecific reactive change of <a href="/facts/Neuroglia/F8BhPmaA">glial cells</a> in response to damage to the <a href="/facts/Central_nervous_system/k8I6To97">central nervous system</a> (CNS). In most cases, gliosis involves the <a href="/facts/Cell_growth/wbArMaJU">proliferation</a> or <a href="/facts/Cellular_adaptation/KP23p64k">hypertrophy</a> of several different types of glial cells, including <a href="/facts/Astrocyte/PBUuHKzS">astrocytes</a>, <a href="/facts/Microglia/fU9dhL72">microglia</a>, and <a href="/facts/Oligodendrocyte/vjyKr3w2">oligodendrocytes</a>. In its most extreme form, the proliferation associated with gliosis leads to the formation of a <a href="/facts/Glial_scar/Kzla0z1W">glial scar</a>.
The process of gliosis involves a series of cellular and molecular events that occur over several days. Typically, the first response to injury is the migration of <a href="/facts/Macrophage/z7hkQu3o">macrophages</a> and local microglia to the injury site. This process, which constitutes a form of gliosis known as microgliosis, begins within hours of the initial CNS injury. Later, after 3–5 days, <a href="/facts/Oligodendrocyte_progenitor/Wlt1wPJW">oligodendrocyte precursor cells</a> are also recruited to the site and may contribute to <a href="/facts/Remyelination/JaWKvC8d">remyelination</a>. The final component of gliosis is <a href="/facts/Astrogliosis/nNk4pcEx">astrogliosis</a>, the proliferation of surrounding astrocytes, which are the main constituents of the glial scar.
Gliosis has historically been given a negative connotation due to its appearance in many CNS diseases and the inhibition of <a href="/facts/Neuroregeneration/2wAxXAF2">axonal regeneration</a> caused by glial scar formation. However, gliosis has been shown to have both beneficial and detrimental effects, and the balance between these is due to a complex array of factors and molecular signaling mechanisms, which affect the reaction of all glial cell types.

Gliosis open-in-new

Gliosis