Mechanobiological insight into brain diseases based on mechanosensitive channels: Common mechanisms and clinical potential.
CNS Neurosci Ther
; 30(6): e14809, 2024 Jun.
Article
en En
| MEDLINE
| ID: mdl-38923822
ABSTRACT
BACKGROUND:
As physical signals, mechanical cues regulate the neural cells in the brain. The mechanosensitive channels (MSCs) perceive the mechanical cues and transduce them by permeating specific ions or molecules across the plasma membrane, and finally trigger a series of intracellular bioelectrical and biochemical signals. Emerging evidence supports that wide-distributed, high-expressed MSCs like Piezo1 play important roles in several neurophysiological processes and neurological disorders.AIMS:
To systematically conclude the functions of MSCs in the brain and provide a novel mechanobiological perspective for brain diseases.METHOD:
We summarized the mechanical cues and MSCs detected in the brain and the research progress on the functional roles of MSCs in physiological conditions. We then concluded the pathological activation and downstream pathways triggered by MSCs in two categories of brain diseases, neurodegenerative diseases and place-occupying damages. Finally, we outlined the methods for manipulating MSCs and discussed their medical potential with some crucial outstanding issues.RESULTS:
The MSCs present underlying common mechanisms in different brain diseases by acting as the "transportation hubs" to transduce the distinct signal patterns the upstream mechanical cues and the downstream intracellular pathways. Manipulating the MSCs is feasible to alter the complicated downstream processes, providing them promising targets for clinical treatment.CONCLUSIONS:
Recent research on MSCs provides a novel insight into brain diseases. The common mechanisms mediated by MSCs inspire a wide range of therapeutic potentials targeted on MSCs in different brain diseases.Palabras clave
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Encefalopatías
/
Mecanotransducción Celular
/
Canales Iónicos
Límite:
Animals
/
Humans
Idioma:
En
Año:
2024
Tipo del documento:
Article