The molecular mechanisms underlying gut microbiota-miRNA interaction in metabolic disorders

Author:

Prukpitikul P.1ORCID,Sirivarasai J.2ORCID,Sutjarit N.2ORCID

Affiliation:

1. Doctor of Philosophy Program in Nutrition, Faculty of Medicine Ramathibodi Hospital and Institute of Nutrition, Mahidol University, Bangkok 10400, Thailand

2. Graduate Program in Nutrition, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok 10400, Thailand

Abstract

Abstract Metabolic disorders are a major global health problem. Gut microbiota not only affect host metabolism through metabolites, inflammatory processes, and microbial-derived extracellular vesicles, but they also modulate the host microRNA, which may impact the host metabolism. Hence, the underlying mechanisms between gut microbiota-microRNA interaction can potentially be a novel alternative strategy for treating metabolic disorders. This review aims to give an update on the latest evidence and current knowledge of the underlying mechanisms of gut microbiota-miRNA interaction, focusing on metabolic homeostasis. Gut microbiota mainly communicate with host microRNA through lipopolysaccharide and secondary microbial metabolites. These signalling messengers circulate around the metabolic organs and modify gene expression through microRNA interference. Interestingly, while intestinal microRNAs play a vital role in both intestinal barrier and gut microbiota homeostasis, the presence of gut microbiota is also required for the proper functioning of intestinal microRNAs, suggesting a cooperative mechanism in intestinal health. Although the correlations between gut microbiota and microRNA have been observed in both mice and humans, a causal relationship should be confirmed. Moreover, further investigation is needed to provide more evidence of a gut microbiota-microRNA interaction to support the possibility of using that axis as a novel therapeutic target to treat metabolic disorders.

Publisher

Brill

Reference91 articles.

1. The gut microbiota metabolite urolithin A inhibits NF-κB activation in LPS stimulated BMDMs;Abdelazeem, K.N.M.

2. RNA-binding protein AUF1 represses Dicer expression;Abdelmohsen, K.

3. Recent trends of metabolic syndrome and its components in military recruits from Saudi Arabia;Al-Shehri, H.A.

4. miR-146a regulates the crosstalk between intestinal epithelial cells, microbial components and inflammatory stimuli;Anzola, A.

5. Extracellular vesicles and pasteurized cells derived from Akkermansia muciniphila protect against high-fat induced obesity in mice;Ashrafian, F.

Cited by 2 articles. 订阅此论文施引文献 订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献

1. Molecular Morbidity Score–Can MicroRNAs Assess the Burden of Disease?;International Journal of Molecular Sciences;2024-07-24

2. The Gut Microbial Regulation of Epigenetic Modification from a Metabolic Perspective;International Journal of Molecular Sciences;2024-06-29

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3