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颗粒物暴露相关肾损伤中的预测性和预防性黏膜通讯

Predictive and Preventive Mucosal Communications in Particulate Matter Exposure-Linked Renal Distress.

作者信息

Moon Yuseok

机构信息

Laboratory of Mucosal Exposome and Biomodulation, Department of Integrative Biomedical Sciences, Biomedical Research Institute, Pusan National University, Yangsan 50612, Korea.

出版信息

J Pers Med. 2021 Feb 11;11(2):118. doi: 10.3390/jpm11020118.

DOI:10.3390/jpm11020118
PMID:33670188
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7916923/
Abstract

Despite research into the epidemiological link between exposure to particulate matter (PM) and renal disorder, there is limited information available on the etiological complexity and molecular mechanisms. Among the early responsive tissues to PM exposure, the mucosal barrier of the airway and alimentary tract may be a crucial source of pathologic mediators leading to inflammatory renal diseases, including chronic kidney disease (CKD). Given that harmful responses and products in mucosa exposed to PM may enter the circulation and cause adverse outcomes in the kidney, the aim of the present review was to address the impact of PM exposure on the mucosal barrier and the vicious feedback cycle in the mucosal environment. In addition to the PM-induced alteration of mucosal barrier integrity, the microbial community has a pivotal role in the xenobiotic metabolism and individual susceptibility to PM toxicity. The dysbiosis-induced deleterious metabolites of PM and nutrients are introduced systemically via a disrupted mucosal barrier, contributing to renal injuries and pathologic severity. In contrast, the progress of mucosa-associated renal disease is counteracted by endogenous protective responses in the mucosa. Along with direct elimination of the toxic mediators, modulators of the mucosal microbial community should provide a promising platform for mucosa-based personalized interventions against renal disorders caused by air pollution.

摘要

尽管对接触颗粒物(PM)与肾脏疾病之间的流行病学联系进行了研究,但关于其病因复杂性和分子机制的信息仍然有限。在对PM暴露的早期反应组织中,气道和消化道的黏膜屏障可能是导致包括慢性肾脏病(CKD)在内的炎症性肾脏疾病的病理介质的关键来源。鉴于暴露于PM的黏膜中的有害反应和产物可能进入循环并在肾脏中导致不良后果,本综述的目的是探讨PM暴露对黏膜屏障的影响以及黏膜环境中的恶性循环。除了PM引起的黏膜屏障完整性改变外,微生物群落在外源物质代谢和个体对PM毒性的易感性中起关键作用。由生态失调引起的PM和营养物质的有害代谢产物通过受损的黏膜屏障被全身吸收,导致肾损伤和病理严重程度。相反,黏膜相关肾脏疾病的进展会被黏膜中的内源性保护反应所抵消。除了直接清除毒性介质外,黏膜微生物群落的调节剂应为基于黏膜的针对空气污染引起的肾脏疾病的个性化干预提供一个有前景的平台。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff51/7916923/3e1523184639/jpm-11-00118-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff51/7916923/36ae5060b854/jpm-11-00118-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff51/7916923/bb54d703a6c4/jpm-11-00118-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff51/7916923/3e1523184639/jpm-11-00118-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff51/7916923/36ae5060b854/jpm-11-00118-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff51/7916923/bb54d703a6c4/jpm-11-00118-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff51/7916923/3e1523184639/jpm-11-00118-g003.jpg

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Size distributions of particle-generated hydroxyl radical (·OH) in surrogate lung fluid (SLF) solution and their potential sources.颗粒生成的羟基自由基(·OH)在替代肺液(SLF)溶液中的尺寸分布及其潜在来源。
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Indoxyl Sulfate, a Uremic Endotheliotoxin.
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