The Role of Oxidative Stress in the Trabecular Meshwork

This article elucidates the pivotal involvement of oxidative stress (OS) in the trabecular meshwork (TM) and its relevance to primary open-angle glaucoma (POAG). The progression of comprehension regarding the impact of free radicals on cellular damage, particularly within mitochondria, is expounded upon, underscoring the diverse origins of reactive oxygen species (ROS). Inflammatory processes and dysregulation contribute to OS, disrupting the delicate balance between ROS generation and antioxidant defense mechanisms. The TM, vital for regulating aqueous humor outflow, exhibits heightened susceptibility due to factors such as elevated metabolic activity, mitochondrial abundance, mechanical stress, UV radiation exposure, and age-related declines in antioxidants. Individuals diagnosed with POAG display diminished antioxidant capacity, rendering them prone to oxidative damage. Essential antioxidative mechanisms, encompassing low molecular weight antioxidants, enzymes, and specific proteins, are pivotal in sustaining optimal outflow resistance. Genetic and protein elements actively participate in cellular responses to OS. MicroRNAs and long noncoding RNAs intricately modulate gene expression under OS conditions, while extracellular vesicles from diverse sources impact TMcells, offering promising therapeutic implications in the context of glaucoma treatment. This article underscores the complex interplay of these factors in preserving ocular health and highlights the potential therapeutic avenues of targeting OS in the management of glaucoma.