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DNA结合/分化蛋白抑制剂与环境毒物:对抑郁性功能障碍发病的基因组影响

Inhibitor of DNA-Binding/Differentiation Proteins and Environmental Toxicants: Genomic Impact on the Onset of Depressive Dysfunction.

作者信息

Avecilla Vincent, Avecilla Andrea

机构信息

Department of Environmental Health Sciences, Robert Stempel College of Public Health & Social Work, Florida International University, Miami, FL 33199, USA.

Celgene Corporation, Summit, NJ 07901, USA.

出版信息

Med Sci (Basel). 2019 Jan 9;7(1):7. doi: 10.3390/medsci7010007.

DOI:10.3390/medsci7010007
PMID:30634536
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6358799/
Abstract

The ongoing growth of the international occurrence of depression and its ability to co-occur with other serious medical disorders, such as heart disease, cancer, diabetes, and Parkinson's disease, is a current public health problem. Inhibitor of DNA-Binding/Differentiation (ID) proteins are part of a group of transcriptional factors that have shown involvement in neurocognitive disorders and, therefore, may have influence on depressive disorders. Previously, it has been established that exposure to environmental estrogenic endocrine disruptors (EEDs), such as polychlorinated biphenyls (PCBs) and bisphenol A (BPA), have played an important role in the modulation of depressive disorders. Hence, based on many studies, we consider the impact of these environmental pollutants on the group of ID proteins and how they impact depressive outcomes. Improved knowledge of how ID proteins interact with depressive disorders, through EED exposure, will contribute essential evidence that can further benefit our public health community with innovative knowledge to prevent these types of mental illnesses.

摘要

抑郁症在国际上的发病率持续上升,且它常与其他严重的医学疾病同时出现,如心脏病、癌症、糖尿病和帕金森病,这是当前的一个公共卫生问题。DNA结合/分化(ID)蛋白抑制剂是一组转录因子的一部分,这些转录因子已被证明与神经认知障碍有关,因此可能对抑郁症产生影响。此前已经确定,接触环境雌激素内分泌干扰物(EEDs),如多氯联苯(PCBs)和双酚A(BPA),在抑郁症的调节中发挥了重要作用。因此,基于众多研究,我们考虑这些环境污染物对ID蛋白组的影响以及它们如何影响抑郁结果。通过EED暴露来更好地了解ID蛋白与抑郁症之间的相互作用,将提供重要证据,从而以创新知识进一步造福我们的公共卫生界,以预防这类精神疾病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6363/6358799/4df10ff4a9aa/medsci-07-00007-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6363/6358799/367fcc3c54bc/medsci-07-00007-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6363/6358799/f65ed38f8012/medsci-07-00007-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6363/6358799/4df10ff4a9aa/medsci-07-00007-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6363/6358799/367fcc3c54bc/medsci-07-00007-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6363/6358799/f65ed38f8012/medsci-07-00007-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6363/6358799/4df10ff4a9aa/medsci-07-00007-g003.jpg

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Sex differences in depression-like behavior and neuroinflammation in rats post-MI: role of estrogens.
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Am J Physiol Heart Circ Physiol. 2018 Nov 1;315(5):H1159-H1173. doi: 10.1152/ajpheart.00615.2017. Epub 2018 Jul 27.
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Neurobiological links between depression and AD: The role of TGF-β1 signaling as a new pharmacological target.抑郁和 AD 之间的神经生物学联系:TGF-β1 信号作为新的药理学靶点的作用。
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