Axonal degeneration is a major contributor to neuronal dysfunction in many neurological conditions and has additional roles in development. It can be triggered by divergent stimuli including mechanical, metabolic, infectious, toxic, hereditary and inflammatory stresses. Axonal mitochondria are an important convergence point as regulators of bioenergetic metabolism, reactive oxygen species (ROS), Ca²⁺ homeostasis and protease activation. The challenges likely to render axonal mitochondria more vulnerable than their cellular counterparts are reviewed, including axonal transport, replenishing nuclear-encoded proteins and maintenance of quality control, fusion and fission in locations remote from the cell body. The potential for mitochondria to act as a decision node in axon loss is considered, highlighting the need to understand the biology of axonal mitochondria and their contributions to degenerative mechanisms for novel therapeutic strategies.

中文翻译：

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线粒体作为轴突退行性刺激的中央传感器

轴索变性是许多神经系统疾病中神经元功能障碍的主要因素，并且在发育中具有其他作用。它可以由不同的刺激触发，包括机械、代谢、感染、毒性、遗传和炎症应激。轴突线粒体是生物能代谢、活性氧 (ROS)、Ca²⁺ 稳态和蛋白酶激活的调节剂的重要汇聚点。审查了可能使轴突线粒体比其细胞对应物更脆弱的挑战，包括轴突运输、补充核编码蛋白以及在远离细胞体的位置保持质量控制、融合和裂变。考虑了线粒体在轴突丢失中充当决策节点的潜力，