Glaucomatous optic nerve damage caused by pathological intraocular pressure elevation is irreversible, and its course is often difficult to control. This group of eye diseases is closely related to biomechanics, and the correlation between glaucoma pathogenesis and mechanical stimulation has been studied in recent decades. The nonselective cation channel Piezo1, the most important known mechanical stress sensor, is a transmembrane protein widely expressed in various cell types. Piezo1 has been detected throughout the eye, and the close relationship between Piezo1 and glaucoma is being confirmed. Pathological changes in glaucoma occur in both the anterior and posterior segments of the eye, and it is of great interest for researchers to determine whether Piezo1 plays a role in these changes and how it functions. The elucidation of the mechanisms of Piezo1 action in nonocular tissues and the reported roles of similar mechanically activated ion channels in glaucoma will provide an appropriate basis for further investigation. From a new perspective, this review provides a detailed description of the current progress in elucidating the role of Piezo1 in glaucoma, including relevant questions and assumptions, the remaining challenging research directions and mechanism-related therapeutic potential.
Keywords: Biomechanics; Glaucoma; Mechanical stress; Mechanically activated ion channels; Piezo1; Retinal ganglion cells; TREK-1; TRPV4; Trabecular meshwork.
© 2022. The Author(s) under exclusive licence to Japan Human Cell Society.