Pilz Yasmine L, Bass Sherry J, Sherman Jerome
State University New York, College of Optometry, New York, USA.
State University New York, College of Optometry, New York, USA.
J Optom. 2017 Oct-Dec;10(4):205-214. doi: 10.1016/j.optom.2016.09.003. Epub 2016 Dec 28.
In recent years, the term mitochondrial optic neuropathy (MON) has increasingly been used within the literature to describe a group of optic neuropathies that exhibit mitochondrial dysfunction in retinal ganglion cells (RGCs). Interestingly, MONs include genetic aetiologies, such as Leber hereditary optic neuropathy (LHON) and dominant optic atrophy (DOA), as well as acquired aetiologies resulting from drugs, nutritional deficiencies, and mixed aetiologies. Regardless of an inherited or acquired cause, patients exhibit the same clinical manifestations with selective loss of the RGCs due to mitochondrial dysfunction. Various novel therapies are being explored to reverse or limit damage to the RGCs. Here we review the pathophysiology, clinical manifestations, differential diagnosis, current treatment, and promising therapeutic targets of MON.
近年来，线粒体视神经病变（MON）这一术语在文献中越来越多地被用于描述一组在视网膜神经节细胞（RGC）中表现出线粒体功能障碍的视神经病变。有趣的是，MON包括遗传性病因，如Leber遗传性视神经病变（LHON）和显性视神经萎缩（DOA），以及由药物、营养缺乏导致的后天性病因和混合性病因。无论病因是遗传性还是后天获得性，患者都会因线粒体功能障碍而出现相同的临床表现，即RGC选择性丧失。目前正在探索各种新的疗法来逆转或限制对RGC的损伤。在此，我们综述了MON的病理生理学、临床表现、鉴别诊断、当前治疗方法以及有前景的治疗靶点。
