Li et al_Source Data.xlsx
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Pathologically altered biomechanical properties of the Schlemm’s canal (SC) inner wall microenvironment were recently validated as the cause for increased outflow resistance in ocular hypertensive glaucoma. However, the involvement of specific mechanotransduction pathways in these disease processes is largely unclear. Here, we demonstrate that YAP/TAZ are central regulators of glaucoma-like SC cell dysfunction in response to extracellular matrix stiffening, and that targeted disruption of YAP/TAZ mechanosignaling attenuates SC cell pathobiology and enhances outflow function.
创建时间：
2023-12-12
