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线粒体可能介导产前环境对自闭症谱系障碍的影响。

Mitochondria May Mediate Prenatal Environmental Influences in Autism Spectrum Disorder.

作者信息

Frye Richard E, Cakir Janet, Rose Shannon, Palmer Raymond F, Austin Christine, Curtin Paul, Arora Manish

机构信息

Barrow Neurological Institute at Phoenix Children's Hospital, Phoenix, AZ 85016, USA.

Department of Applied Ecology, North Carolina State University, Raleigh, NC 27695, USA.

出版信息

J Pers Med. 2021 Mar 18;11(3):218. doi: 10.3390/jpm11030218.

Abstract

We propose that the mitochondrion, an essential cellular organelle, mediates the long-term prenatal environmental effects of disease in autism spectrum disorder (ASD). Many prenatal environmental factors which increase the risk of developing ASD influence mitochondria physiology, including toxicant exposures, immune activation, and nutritional factors. Unique types of mitochondrial dysfunction have been associated with ASD and recent studies have linked prenatal environmental exposures to long-term changes in mitochondrial physiology in children with ASD. A better understanding of the role of the mitochondria in the etiology of ASD can lead to targeted therapeutics and strategies to potentially prevent the development of ASD.

摘要

我们提出,线粒体作为一种重要的细胞器,介导了自闭症谱系障碍(ASD)中疾病的长期产前环境影响。许多增加患ASD风险的产前环境因素会影响线粒体生理学,包括接触有毒物质、免疫激活和营养因素。独特类型的线粒体功能障碍与ASD有关,最近的研究将产前环境暴露与ASD儿童线粒体生理学的长期变化联系起来。更好地理解线粒体在ASD病因学中的作用,可以带来有针对性的治疗方法和策略,有可能预防ASD的发生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b6b/8003154/5c718d55d4b9/jpm-11-00218-g001.jpg

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