Reactive gliosis in traumatic brain injury: a comprehensive review

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378041%3A_____%2F24%3A00586359" target="_blank" >RIV/68378041:_____/24:00586359 - isvavai.cz</a>

Alternative codes found

RIV/00216208:11130/24:10478555

Result on the web

<a href="https://www.frontiersin.org/articles/10.3389/fncel.2024.1335849/full" target="_blank" >https://www.frontiersin.org/articles/10.3389/fncel.2024.1335849/full</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.3389/fncel.2024.1335849" target="_blank" >10.3389/fncel.2024.1335849</a>

Result language

angličtina

Original language name

Reactive gliosis in traumatic brain injury: a comprehensive review

Original language description

Traumatic brain injury (TBI) is one of the most common pathological conditions impacting the central nervous system (CNS). A neurological deficit associated with TBI results from a complex of pathogenetic mechanisms including glutamate excitotoxicity, inflammation, demyelination, programmed cell death, or the development of edema. The critical components contributing to CNS response, damage control, and regeneration after TBI are glial cells-in reaction to tissue damage, their activation, hypertrophy, and proliferation occur, followed by the formation of a glial scar. The glial scar creates a barrier in damaged tissue and helps protect the CNS in the acute phase post-injury. However, this process prevents complete tissue recovery in the late/chronic phase by producing permanent scarring, which significantly impacts brain function. Various glial cell types participate in the scar formation, but this process is mostly attributed to reactive astrocytes and microglia, which play important roles in several brain pathologies. Novel technologies including whole-genome transcriptomic and epigenomic analyses, and unbiased proteomics, show that both astrocytes and microglia represent groups of heterogenic cell subpopulations with different genomic and functional characteristics, that are responsible for their role in neurodegeneration, neuroprotection and regeneration. Depending on the representation of distinct glia subpopulations, the tissue damage as well as the regenerative processes or delayed neurodegeneration after TBI may thus differ in nearby or remote areas or in different brain structures. This review summarizes TBI as a complex process, where the resultant effect is severity-, region- and time-dependent and determined by the model of the CNS injury and the distance of the explored area from the lesion site. Here, we also discuss findings concerning intercellular signaling, long-term impacts of TBI and the possibilities of novel therapeutical approaches. We believe that a comprehensive study with an emphasis on glial cells, involved in tissue post-injury processes, may be helpful for further research of TBI and be the decisive factor when choosing a TBI model.

Czech name

—

Czech description

—

Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

—

OECD FORD branch

30103 - Neurosciences (including psychophysiology)

Project

<a href="/en/project/GA23-06269S" target="_blank" >GA23-06269S: Disturbed regulation of mTOR signaling in glial cells following cerebral ischemia</a><br>

Continuities

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2024

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

Frontiers in Cellular Neuroscience

ISSN

1662-5102

e-ISSN

1662-5102

Volume of the periodical

18

Issue of the periodical within the volume

February

Country of publishing house

CH - SWITZERLAND

Number of pages

43

Pages from-to

1335849

UT code for WoS article

001182251800001

EID of the result in the Scopus database

2-s2.0-85187870410