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与空气污染暴露和自闭症风险相关的代谢途径失调:来自流行病学研究的证据。

Dysregulated metabolic pathways associated with air pollution exposure and the risk of autism: Evidence from epidemiological studies.

机构信息

Department of Population and Public Health Sciences, University of Southern California, Los Angeles, CA, USA.

Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA.

出版信息

Environ Pollut. 2024 Nov 15;361:124729. doi: 10.1016/j.envpol.2024.124729. Epub 2024 Aug 13.

Abstract

Autism spectrum disorder (ASD) is a developmental disorder with symptoms that range from social and communication impairments to restricted interests and repetitive behavior and is the 4th most disabling condition for children aged 5-14. Risk factors of ASD are not fully understood. Environmental risk factors are believed to play a significant role in the ASD epidemic. Research focusing on air pollution exposure as an early-life risk factor of autism is growing, with numerous studies finding associations of traffic and industrial emissions with an increased risk of ASD. One of the possible mechanisms linking autism and air pollution exposure is metabolic dysfunction. However, there were no consensus about the key metabolic pathways and corresponding metabolite signatures in mothers and children that are altered by air pollution exposure and cause the ASD. Therefore, we performed a review of published papers examining the metabolomic signatures and metabolic pathways that are associated with either air pollution exposure or ASD risk in human studies. In conclusion, we found that dysregulated lipid, fatty acid, amino acid, neurotransmitter, and microbiome metabolisms are associated with both short-term and long-term air pollution exposure and the risk of ASD. These dysregulated metabolisms may provide insights into ASD etiology related to air pollution exposure, particularly during the perinatal period in which neurodevelopment is highly susceptible to damage from oxidative stress and inflammation.

摘要

自闭症谱系障碍(ASD)是一种发育障碍,其症状范围从社交和沟通障碍到兴趣受限和重复行为,是 5-14 岁儿童第四大致残疾病。ASD 的风险因素尚未完全了解。环境风险因素被认为在 ASD 流行中起着重要作用。专注于空气污染暴露作为自闭症的早期生命风险因素的研究正在增加,许多研究发现交通和工业排放与 ASD 风险增加之间存在关联。将自闭症与空气污染暴露联系起来的一个可能机制是代谢功能障碍。然而,对于由于空气污染暴露而改变的、与 ASD 相关的关键代谢途径和相应代谢物特征,在母亲和儿童中尚未达成共识。因此,我们对已发表的论文进行了综述,这些论文检查了与人类研究中的空气污染暴露或 ASD 风险相关的代谢组学特征和代谢途径。总之,我们发现,脂质、脂肪酸、氨基酸、神经递质和微生物组代谢的失调与短期和长期的空气污染暴露以及 ASD 风险有关。这些失调的代谢可能为与空气污染暴露相关的自闭症病因学提供了一些见解,特别是在围产期,神经发育非常容易受到氧化应激和炎症的损害。

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