Hogarth Kaley, Tarazi Doorsa, Maynes Jason T
Program in Molecular Medicine, SickKids Research Institute, Toronto, ON, Canada.
Department of Anesthesia and Pain Medicine, Hospital for Sick Children, Toronto, ON, Canada.
Front Neurol. 2023 Jul 18;14:1179823. doi: 10.3389/fneur.2023.1179823. eCollection 2023.
The use of general anesthetics in modern clinical practice is commonly regarded as safe for healthy individuals, but exposures at the extreme ends of the age spectrum have been linked to chronic cognitive impairments and persistent functional and structural alterations to the nervous system. The accumulation of evidence at both the epidemiological and experimental level prompted the addition of a warning label to inhaled anesthetics by the Food and Drug Administration cautioning their use in children under 3 years of age. Though the mechanism by which anesthetics may induce these detrimental changes remains to be fully elucidated, increasing evidence implicates mitochondria as a potential primary target of anesthetic damage, meditating many of the associated neurotoxic effects. Along with their commonly cited role in energy production via oxidative phosphorylation, mitochondria also play a central role in other critical cellular processes including calcium buffering, cell death pathways, and metabolite synthesis. In addition to meeting their immense energy demands, neurons are particularly dependent on the proper function and spatial organization of mitochondria to mediate specialized functions including neurotransmitter trafficking and release. Mitochondrial dependence is further highlighted in the developing brain, requiring spatiotemporally complex and metabolically expensive processes such as neurogenesis, synaptogenesis, and synaptic pruning, making the consequence of functional alterations potentially impactful. To this end, we explore and summarize the current mechanistic understanding of the effects of anesthetic exposure on mitochondria in the developing nervous system. We will specifically focus on the impact of anesthetic agents on mitochondrial dynamics, apoptosis, bioenergetics, stress pathways, and redox homeostasis. In addition, we will highlight critical knowledge gaps, pertinent challenges, and potential therapeutic targets warranting future exploration to guide mechanistic and outcomes research.
在现代临床实践中,全身麻醉剂的使用通常被认为对健康个体是安全的,但在年龄范围两端的暴露与慢性认知障碍以及神经系统持续的功能和结构改变有关。流行病学和实验层面证据的积累促使美国食品药品监督管理局在吸入麻醉剂上添加了警示标签,提醒在3岁以下儿童中使用时需谨慎。尽管麻醉剂可能引发这些有害变化的机制仍有待充分阐明,但越来越多的证据表明线粒体是麻醉损伤的潜在主要靶点,介导了许多相关的神经毒性作用。除了在通过氧化磷酸化产生能量方面的常见作用外,线粒体在其他关键细胞过程中也发挥着核心作用,包括钙缓冲、细胞死亡途径和代谢物合成。除了满足其巨大的能量需求外,神经元尤其依赖线粒体的正常功能和空间组织来介导包括神经递质运输和释放在内的特殊功能。线粒体的依赖性在发育中的大脑中进一步凸显,发育中的大脑需要神经发生、突触发生和突触修剪等时空复杂且代谢成本高昂的过程,这使得功能改变的后果可能影响重大。为此,我们探索并总结了目前对发育中的神经系统中麻醉暴露对线粒体影响的机制理解。我们将特别关注麻醉剂对线粒体动力学、细胞凋亡生物能量学、应激途径和氧化还原稳态的影响。此外,我们将强调关键的知识空白、相关挑战以及值得未来探索以指导机制和结果研究的潜在治疗靶点。