Leber hereditary optic neuropathy (LHON) is a rare, inherited mitochondrial disease. No treatment has shown a clear-cut benefit on a clinically meaningful end-point. Primary open-angle glaucoma (POAG) is a frequent, acquired optic neuropathy. Lowering intraocular pressure (IOP) reduces disease progression. However, current methods to decelerate this progression are recognized as being inadequate. Therefore, there is a clear need to look for new therapeutic approaches. The growing evidence indicates that POAG can also be a mitochondrial optic neuropathy (MON). Several risk elements are common for both diseases and all of them decrease mitochondrial (mt)DNA content. Based on these susceptibility factors and their molecular mechanism, we suggest herein pharmacological therapies targeted to increase mtDNA levels, oxidative phosphorylation (OXPHOS) capability, and mitochondrial energy production as treatments for MONs.

莱伯遗传性视神经病变（LHON）是一种罕见的遗传性线粒体疾病。在临床上有意义的终点上，没有一种治疗方法显示出明显的益处。原发性开角型青光眼（POAG）是一种常见的获得性视神经病变。降低眼内压（IOP）可降低疾病进展。但是，目前公认的使这种进展减速的方法是不充分的。因此，显然需要寻找新的治疗方法。越来越多的证据表明POAG也可能是线粒体视神经病变（MON）。两种疾病都有几种共同的危险因素，所有这些因素都会降低线粒体（mt）DNA含量。基于这些敏感性因素及其分子机制，我们在此建议针对增加mtDNA水平的药理疗法，