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Editors Selection IGR 17-4

Basic Science: Mitochondrial Function

Comment by Miriam Kolko on:

Recent evidence exists on reduced mitochondrial capacity in patients with primary open-angle glaucoma (POAG). In particular, attention has been directed towards impaired complex-I enzyme activity as a potential target to prevent glaucomatous damage. The present study compares complex-1 enzyme activity in lymphoblasts from POAG patients and patients suffering from Leber hereditary optic neuropathy (LHON). While Complex-1 enzyme activity is reduced by 29 % in LHON patients, the same activity in lymphoblasts from patients with POAG is decreased by 18 %. In addition to enzyme activity, the authors demonstrate impaired complex-1 and II ATP synthesis as well as reduced proliferation in lymphoblasts from patients with POAG when grown in galactose media, a condition that forces cells to rely on mitochondrial oxidative phosphorylation. All over, the results strengthen the evidence of reduced mitochondrial capacity as a causative factor for POAG. A limitation of the study is the restricted uniformity of the included subjects. In this matter, it is known that smoking affects mitochondrial function. Furthermore, it is highly probable that mitochondrial implications vary among subjects with low-tension glaucoma compared to patients with high-tension glaucoma. Future studies would benefit from a lesser degree of heterogeneity, which will increase the likelihood of an even more evident involvement of mitochondrial dysfunction in the pathogenesis of POAG. Nevertheless, the authors present very important evidence of impaired mitochondrial respiration in POAG patients. The results are extremely interesting and opens op for new strategies to understand, treat and prevent glaucoma.

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