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Mitochondria May Mediate Prenatal Environmental Influences in Autism Spectrum Disorder

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...

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Autores principales: Frye, Richard E., Cakir, Janet, Rose, Shannon, Palmer, Raymond F., Austin, Christine, Curtin, Paul, Arora, Manish
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8003154/
https://www.ncbi.nlm.nih.gov/pubmed/33803789
http://dx.doi.org/10.3390/jpm11030218
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author Frye, Richard E.
Cakir, Janet
Rose, Shannon
Palmer, Raymond F.
Austin, Christine
Curtin, Paul
Arora, Manish
author_facet Frye, Richard E.
Cakir, Janet
Rose, Shannon
Palmer, Raymond F.
Austin, Christine
Curtin, Paul
Arora, Manish
author_sort Frye, Richard E.
collection PubMed
description 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.
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spelling pubmed-80031542021-03-28 Mitochondria May Mediate Prenatal Environmental Influences in Autism Spectrum Disorder Frye, Richard E. Cakir, Janet Rose, Shannon Palmer, Raymond F. Austin, Christine Curtin, Paul Arora, Manish J Pers Med Review 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. MDPI 2021-03-18 /pmc/articles/PMC8003154/ /pubmed/33803789 http://dx.doi.org/10.3390/jpm11030218 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ).
spellingShingle Review
Frye, Richard E.
Cakir, Janet
Rose, Shannon
Palmer, Raymond F.
Austin, Christine
Curtin, Paul
Arora, Manish
Mitochondria May Mediate Prenatal Environmental Influences in Autism Spectrum Disorder
title Mitochondria May Mediate Prenatal Environmental Influences in Autism Spectrum Disorder
title_full Mitochondria May Mediate Prenatal Environmental Influences in Autism Spectrum Disorder
title_fullStr Mitochondria May Mediate Prenatal Environmental Influences in Autism Spectrum Disorder
title_full_unstemmed Mitochondria May Mediate Prenatal Environmental Influences in Autism Spectrum Disorder
title_short Mitochondria May Mediate Prenatal Environmental Influences in Autism Spectrum Disorder
title_sort mitochondria may mediate prenatal environmental influences in autism spectrum disorder
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8003154/
https://www.ncbi.nlm.nih.gov/pubmed/33803789
http://dx.doi.org/10.3390/jpm11030218
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