Mitochondrial Homeostasis in Trabecular Meshwork Cells: A Potential Mechanism in Glaucoma

Glaucoma is the second leading cause of blindness worldwide, with its core pathological basis being impaired aqueous humor outflow and elevated intraocular pressure due to trabecular meshwork (TM) dysfunction. The structural and functional stability of the TM largely depends on the regulation of TM cells. Mitochondria, as the cellular energy and metabolic hub, play a crucial role in maintaining energy supply, extracellular matrix homeostasis, and cell survival in TM cells. Recent studies have demonstrated that mitochondrial homeostasis imbalance is a key factor in TM cell damage and functional decline, yet no comprehensive review has been published in this field. Therefore, this review comprehensively summarizes the mechanisms of mitochondrial involvement in TM cell dysfunction for the first time. It covers mitochondrial metabolic imbalance, oxidative stress, mitochondrial dynamics disorder, autophagy abnormalities, and mitochondrial genetic and epigenetic regulation. This review aims to reveal the central role of mitochondria in the pathological changes of TM cells and provide new insights and theoretical foundations for future research and intervention strategies.