Davis Chung-Ha O, Marsh-Armstrong Nicholas
a Solomon H. Snyder Department of Neuroscience ; Johns Hopkins University School of Medicine and Hugo W. Moser Research Institute at Kennedy Krieger ; Baltimore , MD USA.
Autophagy. 2014;10(12):2383-4. doi: 10.4161/15548627.2014.981920.
The mitochondrial quality control system regulating mitochondria biogenesis, dynamics, and degradation has been extensively studied because of its roles in normal cell homeostasis and dysfunction due to aging or disease. Mitochondria degradation is generally thought to occur by autophagy and has therefore been viewed as a cell-autonomous process. In a recent study, we demonstrated that a large fraction of retinal ganglion cell mitochondria undergo lysosomal degradation within the astrocytes of the optic nerve head. It will be important to determine whether other neurons with long axons also use transcellular mitophagy, or transmitophagy, as a primary mitochondrial quality control mechanism either under normal physiological conditions or in disease. The elucidation of the underlying molecular mechanisms is necessary to determine whether defects in transmitophagy are involved in pathogenesis and whether it should become a therapeutic target.
由于线粒体质量控制系统在正常细胞稳态以及衰老或疾病导致的功能障碍中所起的作用，对其调节线粒体生物发生、动态变化和降解的研究已广泛开展。线粒体降解通常被认为是通过自噬发生的，因此被视为一个细胞自主过程。在最近的一项研究中，我们证明了很大一部分视网膜神经节细胞线粒体在视神经乳头的星形胶质细胞内经历溶酶体降解。确定其他具有长轴突的神经元在正常生理条件下或疾病状态下是否也将跨细胞线粒体自噬（或传递性自噬）作为主要的线粒体质量控制机制将具有重要意义。阐明潜在的分子机制对于确定传递性自噬缺陷是否参与发病机制以及它是否应成为治疗靶点是必要的。
