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本文引用的文献

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Consideration of pathways for immunotoxicity of per- and polyfluoroalkyl substances (PFAS).考虑全氟和多氟烷基物质 (PFAS) 的免疫毒性途径。
Environ Health. 2023 Feb 22;22(1):19. doi: 10.1186/s12940-022-00958-5.
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Novel Insight into the Mechanisms of Neurotoxicity Induced by 6:6 PFPiA through Disturbing the Gut-Brain Axis.对6:6 PFPiA通过扰乱肠-脑轴诱导神经毒性机制的新见解。
Environ Sci Technol. 2023 Jan 17;57(2):1028-1038. doi: 10.1021/acs.est.2c04765. Epub 2023 Jan 3.
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Inverse relationship between dietary fiber intake and environmental exposure to acrylamide.膳食纤维摄入量与丙烯酰胺环境暴露呈负相关。
Environ Sci Pollut Res Int. 2023 Mar;30(12):35326-35333. doi: 10.1007/s11356-022-24694-y. Epub 2022 Dec 17.
4
Metabolomic, Lipidomic, Transcriptomic, and Metagenomic Analyses in Mice Exposed to PFOS and Fed Soluble and Insoluble Dietary Fibers.暴露于全氟辛烷磺酸(PFOS)并摄入可溶性和不溶性膳食纤维的小鼠的代谢组学、脂质组学、转录组学和宏基因组学分析。
Environ Health Perspect. 2022 Nov;130(11):117003. doi: 10.1289/EHP11360. Epub 2022 Nov 4.
5
Host-microbiome interactions: Gut-Liver axis and its connection with other organs.宿主-微生物组相互作用:肠道-肝脏轴及其与其他器官的联系。
NPJ Biofilms Microbiomes. 2022 Nov 1;8(1):89. doi: 10.1038/s41522-022-00352-6.
6
Trimethylamine, a gut bacteria metabolite and air pollutant, increases blood pressure and markers of kidney damage including proteinuria and KIM-1 in rats.三甲胺,一种肠道细菌代谢物和空气污染物,可增加大鼠的血压和肾脏损伤标志物,包括蛋白尿和 KIM-1。
J Transl Med. 2022 Oct 15;20(1):470. doi: 10.1186/s12967-022-03687-y.
7
Impact of Environmental Pollutants on Gut Microbiome and Mental Health via the Gut-Brain Axis.环境污染物通过肠-脑轴对肠道微生物群和心理健康的影响。
Microorganisms. 2022 Jul 19;10(7):1457. doi: 10.3390/microorganisms10071457.
8
Human exposure to polybrominated diphenyl ethers (PBDEs) through the diet: An update of the scientific literature.人体通过饮食接触多溴二苯醚(PBDEs):科学文献的最新更新。
Food Chem Toxicol. 2022 Sep;167:113322. doi: 10.1016/j.fct.2022.113322. Epub 2022 Jul 22.
9
Multiomics analysis of the impact of polychlorinated biphenyls on environmental liver disease in a mouse model.多组学分析多氯联苯对小鼠模型环境性肝病的影响
Environ Toxicol Pharmacol. 2022 Aug;94:103928. doi: 10.1016/j.etap.2022.103928. Epub 2022 Jul 6.
10
The Role of Fecal Microbiota in Liver Toxicity Induced by Perfluorooctane Sulfonate in Male and Female Mice.粪菌在雄性和雌性小鼠中全氟辛烷磺酸诱导的肝毒性中的作用。
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由持久性有机污染物和营养干预引起的炎症和心血管代谢疾病:多器官相互作用的影响。

Inflammation and cardiometabolic diseases induced by persistent organic pollutants and nutritional interventions: Effects of multi-organ interactions.

机构信息

Jiangsu Key Laboratory of Neuropsychiatric Diseases and College of Pharmaceutical Sciences, Soochow University, Suzhou, Jiangsu, China; Irish Centre for Vascular Biology, School of Pharmacy & Biomolecular Sciences, Royal College of Surgeons in Ireland, Ireland.

Jiangsu Key Laboratory of Neuropsychiatric Diseases and College of Pharmaceutical Sciences, Soochow University, Suzhou, Jiangsu, China.

出版信息

Environ Pollut. 2023 Dec 15;339:122756. doi: 10.1016/j.envpol.2023.122756. Epub 2023 Oct 14.

DOI:10.1016/j.envpol.2023.122756
PMID:37844865
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10842216/
Abstract

The development and outcome of inflammatory diseases are associated with genetic and lifestyle factors, which include chemical and nonchemical stressors. Persistent organic pollutants (POPs) are major groups of chemical stressors. For example, dioxin-like polychlorinated biphenyls (PCBs), per- and polyfluoroalkyl substances (PFASs), and polybrominated diphenyl ethers (PBDEs) are closely associated with the incidence of inflammatory diseases. The pathology of environmental chemical-mediated inflammatory diseases is complex and may involve disturbances in multiple organs, including the gut, liver, brain, vascular tissues, and immune systems. Recent studies suggested that diet-derived nutrients (e.g., phytochemicals, vitamins, unsaturated fatty acids, dietary fibers) could modulate environmental insults and affect disease development, progression, and outcome. In this article, mechanisms of environmental pollutant-induced inflammation and cardiometabolic diseases are reviewed, focusing on multi-organ interplays and highlighting recent advances in nutritional strategies to improve the outcome of cardiometabolic diseases associated with environmental exposures. In addition, advanced system biology approaches are discussed, which present unique opportunities to unveil the complex interactions among multiple organs and to fuel the development of precision intervention strategies in exposed individuals.

摘要

炎症性疾病的发生和发展与遗传和生活方式因素有关,其中包括化学和非化学应激源。持久性有机污染物(POPs)是化学应激源的主要类别。例如,类二恶英多氯联苯(PCBs)、全氟和多氟烷基物质(PFASs)以及多溴联苯醚(PBDEs)与炎症性疾病的发病率密切相关。环境化学介导的炎症性疾病的病理十分复杂,可能涉及多个器官的紊乱,包括肠道、肝脏、大脑、血管组织和免疫系统。最近的研究表明,饮食来源的营养素(例如植物化学物质、维生素、不饱和脂肪酸、膳食纤维)可以调节环境刺激并影响疾病的发展、进展和结果。本文综述了环境污染物引起的炎症和心血管代谢疾病的机制,重点关注多器官相互作用,并强调了营养策略在改善与环境暴露相关的心血管代谢疾病方面的最新进展。此外,还讨论了先进的系统生物学方法,这些方法为揭示多个器官之间的复杂相互作用以及为暴露个体开发精准干预策略提供了独特的机会。