Mitochondrial insufficiencies and neuroprotection in glaucoma

Antihypertensive management has long been the mainstay of treatment for glaucoma. Despite contemporary treatments, many patients still experience disease progression, with some ultimately losing vision. The purpose of this review is to demonstrate how derangements in mitochondrial biology underpin the pathophysiology of glaucoma, and to explore emerging therapeutic options.

Literature searches were performed using multiple databases, aiming to identify recent developments in the scientific knowledge surrounding mitochondrial biology and glaucoma. Key words used in the primary literature search included combinations of "glaucoma", "mitochondria", "oxidative stress", "metabolism", "inflammation", "transport" and "genetics". Additional database searches were performed to further explore specific details identified in the primary search.

Recent research points to mitochondrial insufficiencies as a primary culprit in the pathophysiology of glaucoma. Dysfunction of mitochondria occurs in a multitude of ways, and is an integral component of neuroinflammation, metabolic compromise, and disruption of axonal transport. This in part results from accumulated genetic factors, leading to generation of superoxides that damage retinal ganglion cells resulting in neurodegeneration of the optic nerve. Defects in mitochondrial biology among a range of ocular cell types contribute to the progression of glaucoma. With this understanding, emerging treatments targeting mitochondria, including gene therapies, tunneling nanotubules, and pharmacotherapeutics which enhance mitochondrial function and reduce oxidative stress, are likely the future of glaucoma management.

By targeting mitochondrial insufficiencies as a root cause of glaucoma in addition to managing intraocular pressure, this new approach offers hope for preventing vision loss and potentially curing glaucoma.