Piezo2 Contributes to Traumatic Brain Injury by Activating the RhoA/ROCK1 Pathways
ROCK1
DOI:
10.1007/s12035-024-04058-y
Publication Date:
2024-02-22T20:02:20Z
AUTHORS (7)
ABSTRACT
Traumatic brain injury (TBI) can lead to short-term and long-term physical cognitive impairments, which have significant impacts on patients, families, society. Currently, treatment outcomes for this disease are often unsatisfactory, due at least in part the fact that molecular mechanisms underlying development of TBI largely unknown. Here, we observed upregulation Piezo2, a key mechanosensitive ion channel protein, injured tissue mouse model induced by controlled cortical impact. Pharmacological inhibition genetic knockdown Piezo2 after attenuated neuronal death, edema, necrosis, deficits neural function function. Mechanistically, increase expression contributed TBI-induced death subsequent production TNF-α IL-1β, likely through activation RhoA/ROCK1 pathways central nervous system. Our findings suggest is player potential therapeutic target TBI.
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