Circadian rhythms in most living organisms are regulated by light and synchronized to an endogenous biological clock. The circadian clock machinery is also critically involved in regulating and fine-tuning neurodevelopmental processes. Circadian disruption during embryonic development can impair crucial phases of neurodevelopment. This can contribute to neurodevelopmental disorders like autism spectrum disorder (ASD) in the offspring. Increasing evidence from studies showing abnormalities in sleep and melatonin as well as genetic and epigenetic changes in the core elements of the circadian pathway indicate a pivotal role of circadian disruption in ASD. However, the underlying mechanistic basis through which the circadian pathways influence the risk and progression of ASD are yet to be fully discerned. Well-recognized mechanistic pathways in ASD include altered immune-inflammatory, nitro oxidative stress, neurotransmission and synaptic plasticity, and metabolic pathways. Notably, all these pathways are under the control of the circadian clock. It is thus likely that a disrupted circadian clock will affect the functioning of these pathways. Herein, we highlight the possible mechanisms through which aberrations in the circadian clock might affect immune-inflammatory, nitro-oxidative, metabolic pathways, and neurotransmission, thereby driving the neurobiological sequelae leading to ASD.

中文翻译：

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昼夜节律紊乱和自闭症谱系障碍风险：免疫炎症、氧化应激、代谢和神经递质通路的作用

大多数生物体的昼夜节律由光调节并与内源性生物钟同步。生物钟机制也关键参与调节和微调神经发育过程。胚胎发育过程中的昼夜节律紊乱会损害神经发育的关键阶段。这可能导致后代的神经发育障碍，如自闭症谱系障碍 (ASD)。越来越多的研究表明睡眠和褪黑激素异常以及昼夜节律通路核心元素的遗传和表观遗传变化表明昼夜节律紊乱在 ASD 中的关键作用。然而，昼夜节律通路影响 ASD 风险和进展的潜在机制基础尚待充分认识。ASD 中公认的机制途径包括改变的免疫炎症、硝基氧化应激、神经传递和突触可塑性以及代谢途径。值得注意的是，所有这些途径都在生物钟的控制之下。因此，被打乱的生物钟很可能会影响这些通路的功能。在这里，我们强调了生物钟异常可能影响免疫炎症、硝基氧化、代谢途径和神经传递的可能机制，从而驱动导致 ASD 的神经生物学后遗症。因此，被打乱的生物钟很可能会影响这些通路的功能。在这里，我们强调了生物钟异常可能影响免疫炎症、硝基氧化、代谢途径和神经传递的可能机制，从而驱动导致 ASD 的神经生物学后遗症。因此，被打乱的生物钟很可能会影响这些通路的功能。在这里，我们强调了生物钟异常可能影响免疫炎症、硝基氧化、代谢途径和神经传递的可能机制，从而驱动导致 ASD 的神经生物学后遗症。