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From death to rebirth: How do reactive astrocytes reshape the brain after injury?
The process of glial scar formation (gliosis) is one mechanism of cellular response following injury to the central nervous system (CNS). This process is similar to scarring in other organs and tissues and is a mechanism by which the body protects and initiates the healing process after injury. However, glial scar formation has been shown to have both beneficial and harmful effects in the context of neurodegenerative diseases.
During this process, many neurodevelopmental inhibitory factors are secreted by cells within the glial scar, the production of which prevents full physical and functional recovery of the central nervous system after injury or disease.
Specifically, glial scars are composed of several components, among which reactive astrocytes are the major cellular component. These astrocytes undergo morphological changes after injury, enhance their processes and synthesize glial fibrillary acidic protein (GFAP). GFAP is an important intermediate filament protein that helps astrocytes synthesize more cytoskeletal structures and extend their pseudopodia.
Ultimately, astrocytes form a dense network that fills the gaps created by dead or dying neuronal cells, a process called gliosis.
In the post-injury environment, microglia, as another important cell type, rapidly activate and secrete a variety of cytokines, bioactive lipids, coagulation factors, and nerve growth factors. These molecules have an important influence on the expression of microglia relative to the wound location, and usually the microglia closest to the wound secrete the most active molecules.
Beneficial and harmful effects of glial scar
The ultimate function of the glial scar is to reestablish the physical and chemical integrity of the central nervous system. It forms a barrier that seals the boundary between nerves and non-neural tissue, helping to prevent microbial infection and further cellular damage.
However, the presence of glial scars also prevents neuronal regeneration, and damaged axons often encounter both physical and chemical obstacles when trying to cross the wound.
Molecular inducers of glial scar formation
The formation of glial scar is a complex process involving multiple molecular mediators. Molecules such as transforming growth factor β (TGF-β), interleukins (IL) and cytokines play an important role in this process. In particular, TGF-β-1 and TGF-β-2 can directly stimulate the proliferation of astrocytes and other cells.
Reduction of TGFβ-1 and TGFβ-2 has shown potential to reduce glial scar formation, which is critical for improving recovery after central nervous system injury.
Techniques to inhibit glial scar formation
The medical community has developed a variety of technologies to inhibit the formation of glial scars, such as the use of Olomoucine, a cell cycle-dependent kinase inhibitor that can reduce the proliferation of astrocytes.
The combined use of these techniques, especially in combination with neuroregeneration techniques, shows potential in promoting functional recovery.
Treatment or removal of glial scars
Degrading glial scars through the use of drugs such as Chondroitinase ABC is expected to promote recovery after spinal cord injury, especially when it is combined with other technologies.
In general, the formation of glial scar is a double-edged sword that can protect or hinder the recovery of the central nervous system. How will future research help us understand and manipulate this process to promote true neural reconstruction?
