Targeting mitochondrial dysfunction: Innovative strategies to combat glaucoma neuroinflammation

Abstract

Glaucomatous optic neuropathy represents a prevalent optic nerve degenerative disease. Neuroinflammation is recognized as a significant mechanism underlying optic nerve damage in glaucoma; however, the precise mechanisms driving neuroinflammation remain largely elusive. Existing studies have indicated that microglia-driven neuroinflammation is pivotal for neuroinflammation onset and progression. Mitochondrial dysfunction, encompassing mitochondrial DNA (mtDNA) damage, metabolic deficiencies, and quality control impairments, is upstream of microglial activation and neuroinflammation. Thus, a deeper comprehension of the link between mitochondrial dysfunction and microglial activation in glaucoma may provide valuable insights into the underlying pathogenesis. As a result of these findings, promising avenues for developing effective interventions to mitigate optic nerve damage and preserve visual function in glaucoma patients have been identified.