Astrocytic TRPV4 Channels and Their Role in Brain Ischemia
Jazyk angličtina Země Švýcarsko Médium electronic
Typ dokumentu časopisecké články, přehledy
Grantová podpora
LX22NPO5107 (MEYS)
EU-Next Generation EU
20-05770S
Czech Science Foundation
956325
Funding agency - European Union's Horizon 2020
PubMed
37108263
PubMed Central
PMC10138480
DOI
10.3390/ijms24087101
PII: ijms24087101
Knihovny.cz E-zdroje
- Klíčová slova
- Ca2+ signaling, TRPV4, astrocytes, glia, ischemia,
- MeSH
- astrocyty * metabolismus MeSH
- centrální nervový systém metabolismus MeSH
- cerebrální infarkt MeSH
- ischemie mozku * metabolismus MeSH
- kationtové kanály TRPV * metabolismus MeSH
- lidé MeSH
- mozek metabolismus MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
- Názvy látek
- kationtové kanály TRPV * MeSH
- TRPV4 protein, human MeSH Prohlížeč
Transient receptor potential cation channels subfamily V member 4 (TRPV4) are non-selective cation channels expressed in different cell types of the central nervous system. These channels can be activated by diverse physical and chemical stimuli, including heat and mechanical stress. In astrocytes, they are involved in the modulation of neuronal excitability, control of blood flow, and brain edema formation. All these processes are significantly impaired in cerebral ischemia due to insufficient blood supply to the tissue, resulting in energy depletion, ionic disbalance, and excitotoxicity. The polymodal cation channel TRPV4, which mediates Ca2+ influx into the cell because of activation by various stimuli, is one of the potential therapeutic targets in the treatment of cerebral ischemia. However, its expression and function vary significantly between brain cell types, and therefore, the effect of its modulation in healthy tissue and pathology needs to be carefully studied and evaluated. In this review, we provide a summary of available information on TRPV4 channels and their expression in healthy and injured neural cells, with a particular focus on their role in ischemic brain injury.
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