**3. Astrocyte-induced pathogenesis**

ASTROCYTIC cells are central homeostatic and protective cells of the nerves, and every kind of astrocyte plays an integral part in neuropathological changes. Hence, the decline in nerve cells or astrocytes causes a disease-permissive landscape and

**Figure 2.**

*Astroglial asthenia/atrophy and astrogliosis in neuropathology.*

**Figure 3.**

*Hypoxia and HIF-1*α *stabilization in brain.*

triggers nerve cell malfunction, nerve cell death, and nerve cell deficiency. Glia cells are essential for sustaining nerve function, and nerves survive bodily procedures and pathology [6]. Most essential findings concerning astrocyte's functional significance depend on the dead animal model research. It's given a durable but incomplete base for a complete astrocyte role in physiopathology [7]. They are categorized into three kinds that are reactive astrogliosis, Astro-degeneration with astroglial atrophy, and pathological remodelling and loss of function of astrocytes. Altogether these pathological feedbacks proceed together. It's categorized on the base of neuroanatomical and severity. According to neuroanatomical, astrocytes are further distributed into isomorphic and isomorphic astrogliosis [8]. The isomorphic astrogliosis conserves astroglial defensive areas that are changeable.

In contrast, anisomorphic astrogliosis continues through the destruction of the defensive regions, cell relocation and territorial overlap, development of astroglial palisades, and eventually scar formation. While in severity, astrogliosis is categorized *Impact of Hypoxia on Astrocyte Induced Pathogenesis DOI: http://dx.doi.org/10.5772/intechopen.106263*

#### **Figure 4.**

*Role of hypoxia in activation of inflammatory pathway.*

into slight to adequate astrogliosis, severe diffuse astrogliosis and severe astrogliosis by dense scar development [9]. Astroglial atrophy is mainly noticeable in major psychiatric illnesses. For example, schizophrenia, a primary depressing condition, Wernicke–Korsakoff encephalopathy, and addictive disorders decrease the storing concentration of astrocytic cells. The conclusion is furthermost particularly accompanied by glutamate-glutamine shuttle and glutamate homeostasis; both are impaired in these conditions [10]. It promotes several leukodystrophies, especially Alexander disease, megalocephalic leukoencephalopathy with subcortical lumps or disappearing white matter disease, in which the astrocyte-pathy pledges destruction of the white matter [11]. It also describes mesial temporal lobe epilepsy, in which astrocytes obtain abnormal cell structure, decreases gap junction coupling, and decrease Kir4.1 channel expression; these alterations weaken K+ homeostasis, contributing to seizure start [12].
