Mitochondrial dysfunction is the impaired ability of mitochondria, the organelles responsible for producing cellular energy, to carry out their normal functions. When mitochondria do not generate adenosine triphosphate efficiently, cells experience energy shortfalls and elevated oxidative stress, which can damage pr…
Mitochondrial dysfunction is the impaired ability of mitochondria, the organelles responsible for producing cellular energy, to carry out their normal functions. When mitochondria do not generate adenosine triphosphate efficiently, cells experience energy shortfalls and elevated oxidative stress, which can damage proteins, lipids, and DNA. Because tissues with high energy demands are especially vulnerable, mitochondrial dysfunction is implicated in a broad range of conditions, including neurodegenerative and metabolic disorders and age-related decline. In the eye, retinal ganglion cells and the optic nerve have substantial energy requirements, and disturbances in mitochondrial energy production and oxidative balance are of interest in understanding optic neuropathies. Within the scope of the International Journal of Glaucoma, mitochondrial dysfunction is relevant to mechanisms of retinal ganglion cell stress, optic nerve health, and the cellular pathways that may contribute to glaucomatous damage. Research in this area considers how energy metabolism, oxidative stress, and mitochondrial integrity relate to the survival of the cells most affected in glaucoma. This page gathers peer-reviewed, open-access research relevant to mitochondrial dysfunction and its role in cellular and ocular health.
12 peer-reviewed articles, ranked by relevance. Each links to its DOI.
The 12 articles above have been cited 25 times in the scholarly literature. Citation data via OpenAlex and Crossref, updated Jun 2026.
A sample of recent works citing this journal's research on Mitochondrial Dysfunction, linking to each citing work.