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- Title
Mechanical properties of the brain: Focus on the essential role of Piezo1‐mediated mechanotransduction in the CNS.
- Authors
Zheng, Qingcui; Liu, Hailin; Yu, Wen; Dong, Yao; Zhou, Lanqian; Deng, Wenze; Hua, Fuzhou
- Abstract
Background: The brain is a highly mechanosensitive organ, and changes in the mechanical properties of brain tissue influence many physiological and pathological processes. Piezo type mechanosensitive ion channel component 1 (Piezo1), a protein found in metazoans, is highly expressed in the brain and involved in sensing changes of the mechanical microenvironment. Numerous studies have shown that Piezo1‐mediated mechanotransduction is closely related to glial cell activation and neuronal function. However, the precise role of Piezo1 in the brain requires further elucidation. Objective: This review first discusses the roles of Piezo1‐mediated mechanotransduction in regulating the functions of a variety of brain cells, and then briefly assesses the impact of Piezo1‐mediated mechanotransduction on the progression of brain dysfunctional disorders. Conclusions: Mechanical signaling contributes significantly to brain function. Piezo1‐mediated mechanotransduction regulates processes such as neuronal differentiation, cell migration, axon guidance, neural regeneration, and oligodendrocyte axon myelination. Additionally, Piezo1‐mediated mechanotransduction plays significant roles in normal aging and brain injury, as well as the development of various brain diseases, including demyelinating diseases, Alzheimer's disease, and brain tumors. Investigating the pathophysiological mechanisms through which Piezo1‐mediated mechanotransduction affects brain function will give us a novel entry point for the diagnosis and treatment of numerous brain diseases.
- Subjects
ION channels; MECHANOTRANSDUCTION (Cytology); NEURAL stem cells; OLIGODENDROGLIA; ALZHEIMER'S disease; TISSUE mechanics; CELL migration; NEURONAL differentiation
- Publication
Brain & Behavior, 2023, Vol 13, Issue 9, p1
- ISSN
2162-3279
- Publication type
Article
- DOI
10.1002/brb3.3136