ArticleMolecular neurobiology2024
Piezo2 Contributes to Traumatic Brain Injury by Activating the RhoA/ROCK1 Pathways.
Article in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 10 citations in OpenAlex.
- Dynamic control of cell state transitions during tissue morphogenesis.The EMBO journal · 2026Review
- Targeting the Mechanosensitive Channel Piezo2 Alleviates Intracerebral Hemorrhage-induced Brain Injury by Modulating ER Stress.Translational stroke research · 2026Article
- Sympathetic Overactivation Drives Neurogenic Alveolar Epithelial Pyroptosis via the PIEZO2-ER Stress Pathway in Acute Lung Injury Following Intracerebral Hemorrhage.CNS neuroscience & therapeutics · 2026Article
- The Dynamics of Neuroinflammation in Traumatic Brain Injury: Molecular Markers Useful for Establishing the Post-Traumatic Interval in Forensic Practice.International journal of molecular sciences · 2026Review
- Tuina ameliorates sleep disturbances in PCPA-treated rats through Piezo1-mediated calcium signaling.Frontiers in pharmacology · 2026Article
- The research progress into cellular mechanosensitive ion channels mediating cancer pain.Channels (Austin, Tex.) · 2025Review
- The brain-heart axis: integrative cooperation of neural, mechanical and biochemical pathways.Nature reviews. Cardiology · 2025Review
- Cellular mechanisms of traumatic brain injury.npj biological physics and mechanics · 2025Review
- Piezo channels in JG cells do not regulate renin expression or renin release to the circulation.Clinical science (London, England : 1979) · 2024Article
- Article
- Alternation of gene expression in brain-derived exosomes after cerebral ischemic preconditioning in mice.Heliyon · 2024Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) can lead to short-term and long-term physical and cognitive impairments, which have significant impacts on patients, families, and society. Currently, treatment outcomes for this disease are often unsatisfactory, due at least in part to the fact that the molecular mechanisms underlying the development of TBI are largely unknown. Here, we observed significant upregulation of Piezo2, a key mechanosensitive ion channel protein, in the injured brain tissue of a mouse model of TBI induced by controlled cortical impact. Pharmacological inhibition and genetic knockdown of Piezo2 after TBI attenuated neuronal death, brain edema, brain tissue necrosis, and deficits in neural function and cognitive function. Mechanistically, the increase in Piezo2 expression contributed to TBI-induced neuronal death and subsequent production of TNF-α and IL-1β, likely through activation of the RhoA/ROCK1 pathways in the central nervous system. Our findings suggest that Piezo2 is a key player in and a potential therapeutic target for TBI.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.