Abstract:

Trabecular meshwork（TM） is the target tissue of glaucoma in the anterior chamber. TM cell dysfunction could lead to elevated intraocular pressure. Recently,  lots of researches found that mitochondrial dysfunction and oxidative stress play the key roles in TM injury. Mitochondria is an important place in aerobic respiration of the cell and it’s dysfunction would end up with reduced intracellular ATP synthesis and increased reactive oxygen species (ROS). Excessive accumulation of ROS may contribute to mitochondrial DNA damage and further injury of the mitochondrial,   in turn,  generate more ROS. The release of ROS injures the mitochondria lead to the release of cytochrome C,  which activated caspase pathway and then induction of cell apoptosis. In addition，oxidative stress caused by mitochondrial dysfunction would contribute to cell death of TM by causing macromolecular substances injury,  inducing inflammation or mediating lysosome dysfunction.