Modulation of mitochondrial behavior in unmyelinated axon of glaucomatous optic neuropathy.

在青光眼眼，观察到视神经板层区域周围的Mitotracker标记的线粒体减少。在脑水肿线粒体中观察到硫氧还蛋白2（Trx 2）水平显著降低。视神经损伤后，线粒体凋亡诱导因子（AIF）的变化轻微减少，而轴浆AIF的变化显著增加。此外，在眼压升高后，在RGC中观察到核AIF的显著增加。因此，降低线粒体膜电位和随后的AIF易位参与了脑水肿性神经变性。此外，通过抑制AIF易位来调节线粒体可能成为治疗神经退行性疾病（如青光眼）的新策略。

A decrease in Mitotracker labeled mitochondria around lamina area at the optic nerve was observed in glaucomatous eye. Significant decrease in thioredoxin2 (Trx2) level was observed in the glaucomatous mitochondria. The change of mitochondrial apoptosis-inducing factor (AIF) was slightly decreased, whereas significant increase in axoplasmic AIF was observed in the glaucomatous optic nerve. Furthermore, substantial increase in nucleus AIF was observed in RGCs after IOP elevation. Thus, a decreased mitochondrial membrane potential and subsequent AIF translocation were involved in glaucomatous neurodegeneration. Furthermore, modulation of mitochondria through the inhibition of AIF translocation may become new strategy for neurodegenerative disease, such as glaucoma.