Table 1.
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.