Activation and Role of Astrocytes in Ischemic Stroke

Abstract

Ischemic stroke refers to the disorder of blood supply of local brain tissue caused by various reasons. It has high morbidity and mortality worldwide. Astrocytes are the most abundant glial cells in the central nervous system (CNS). They are responsible for the homeostasis, nutrition, and protection of the CNS and play an essential role in many nervous system diseases’ physiological and pathological processes. After stroke injury, astrocytes are activated and play a protective role through the heterogeneous and gradual changes of their gene expression, morphology, proliferation, and function, that is, reactive astrocytes. However, the position of reactive astrocytes has always been a controversial topic. Many studies have shown that reactive astrocytes are a double-edged sword with both beneficial and harmful effects. It is worth noting that their different spatial and temporal expression determines astrocytes’ various functions. Here, we comprehensively review the different roles and mechanisms of astrocytes after ischemic stroke. In addition, the intracellular mechanism of astrocyte activation has also been involved. More importantly, due to the complex cascade reaction and action mechanism after ischemic stroke, the role of astrocytes is still difficult to define. Still, there is no doubt that astrocytes are one of the critical factors mediating the deterioration or improvement of ischemic stroke.

Anti-Inflammatory Effect of Beta-Caryophyllene Mediated by the Involvement of TRPV1, BDNF and trkB in the Rat Cerebral Cortex after Hypoperfusion/Reperfusion

“…The TRPV1 expression in the CNS has been investigated in numerous previous studies using different techniques; however, the available information concerning its cellular localization and regional distribution is still contradictory [ 48 , 49 , 71 , 72 , 73 , 74 , 75 , 76 ]. On the other hand, there is consensus regarding the involvement of TRPV1 in functions that, on the base of its multimodal activation, differ depending on the neuronal system/neuropathological condition considered [ 50 , 77 ].…”

“…Indeed, though with a time longer than that of our BCCAO/R model, it has been shown that the inflammatory milieu generated by 2.5 h of ischemic brain injury stimulated a strong astroglial response. This response was featured by cell hypertrophy and hyperplasia [ 77 , 80 ], and it was suggested that it may lead to an increased expression of GFAP, partly because the number of GFAP-positive astrocytes increases [ 81 ].…”

Research Progress on the Role of RNA m6A Modification in Glial Cells in the Regulation of Neurological Diseases

“…In addition, astrocytes are activated under P2Y1 stimulation for dual roles with astrocyte-mediated excitatory amino acid transporter (EAAT) disorder and damage to aquaporin4, leading to glutamate excitatory cytotoxicity, cerebral blood flow disorder, and cerebral edema. Inflammatory factors also inhibit the proliferation and differentiation of cells of the OL lineage, resulting in demyelination and worsening prognosis [ 88 , 89 ].…”

Research progress on astrocyte autophagy in ischemic stroke

“…In the malignant secondary process of cerebral ischemic injury, astrocytes perform different functions at different stages, which are affected by many factors and mechanisms. Astrocytes activated by ischemic injury become reactive astrocytes, and under the influence of oxidative stress, inflammation, apoptosis, and other mechanisms caused by cerebral ischemic injury, they play a role in alleviating oxidative stress, releasing neurotrophic factors, producing excitatory toxicity, triggering inflammation, and glial scar formation ( 108 ). Astrocyte autophagy is one of the important regulatory mechanisms that plays an important role in the crosstalk between autophagy and other mechanisms.…”