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Mitophagy is the sole mechanism for neurons to eliminate superfluous or damaged mitochondria. Although the critical implications of mitophagy have been emphasized in a variety of neurological disorders, it remains ambiguous how neurons control the quality of axonal mitochondria. By employing an oxygen-glucose-deprivation and reperfusion (OGD-Rep) model in cultured neurons, our recent results clearly documented the prompt recovery of retrograde transport of axonal mitochondria to neuronal soma. Moreover, by selectively labeling axonal mitochondria, we found that these axonal mitochondria appear in neuronal soma and are eliminated via autophagosomes in priority. This mitochondrial movement from axon to soma has a critical contribution to overall neuronal mitophagy under ischemia. Because forced expression of an anchoring protein, SNPH (Syntaphilin), significantly blocks mitophagy, and aggravates mitochondrial dysfunction and neuronal injury. Conversely, promoted retrograde mitochondrial movement facilitates neuronal mitophagy and attenuates ischemic neuronal demise. In conclusion, we propose stimulating the somatic autophagy of axonal mitochondria after ischemic insults. These findings may provide further insight into how neurons control the mitochondrial quality in pathological conditions and offer novel strategies to cure neurological disorders.
This article was published in the following journal.
Neurons are specialized cells with complex and extended architecture and high energy requirements. Energy in the form of adenosine triphosphate, produced essentially by mitochondrial respiration, is n...
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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease affecting the central and peripheral motor neurons, characterized by the rapidity of its evolution (median survival of 3 ...
The purpose of this study is to determine whether a relationship exists between gene deletion(s) specific to the mitochondrial electron transport chain and presentation of clinical charact...
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Formation of neuronal processes (AXONS; NEURITES) toward a target cell.
UBIQUITIN-like modifier proteins that function in CYTOPLASM to VACUOLE transport (Cvt), vesicle transport within the GOLGI APPARATUS, and AUTOPHAGOSOME biogenesis. They are also required for selective autophagic degradation of the nucleus (nucleophagy) and MITOPHAGY.
Cytochromes of the c type that are found in eukaryotic MITOCHONDRIA. They serve as redox intermediates that accept electrons from MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX III and transfer them to MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX IV.
The application of repeated, brief periods of vascular occlusion at the onset of REPERFUSION to reduce REPERFUSION INJURY that follows a prolonged ischemic event. The techniques are similar to ISCHEMIC PRECONDITIONING but the time of application is after the ischemic event instead of before.
The directed transport of ORGANELLES and molecules along nerve cell AXONS. Transport can be anterograde (from the cell body) or retrograde (toward the cell body). (Alberts et al., Molecular Biology of the Cell, 3d ed, pG3)