Table 1.

BAK, TGFβ2, and POAG Induce Similar Changes in TM Tissue/HTM Cells

BAK exposure-HTM cells and animal models	TGFβ2 exposure-HTM cells and animal models	TM of POAG patients
Loss of cells	Loss of cells	Loss of cells
Increased: accumulation of ECM, apoptosis, ROS, inflammatory markers, fibronectin	Increased: accumulation of ECM, apoptosis, ROS, inflammatory markers, fibronectin	Increased: accumulation of ECM, apoptosis, ROS, inflammatory markers, fibronectin
Changes in the cytoskeleton	Changes in the cytoskeleton	Changes in the cytoskeleton
Cellular senescence-associated changes	Cellular senescence-associated changes	Cellular senescence-associated changes
Decreased outflow	Decreased outflow	Decreased outflow
??????	Presence of CLANS	Presence of CLANS

BAK might play a role in the pathogenesis of POAG.

BAK, benzalkonium chloride; TGFβ2, transforming growth factor beta 2; POAG, primary open-angle glaucoma; TM, trabecular meshwork; HTM, human trabecular meshwork; ECM, extracellular matrix; ROS, reactive oxygen species.

??????, no data currently available.