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MiRNA-21 Regulates Multiple Factors in the Pathogenesis of IBD: A Literature Review MiRNA-21调控IBD发病机制中的多因素:文献综述
Miriam Basta, Christian Guindi, Sherry Erian
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引用次数: 0
MiRNA-21 Regulates Multiple Factors in the Pathogenesis of IBD: A Literature Review MiRNA-21调控IBD发病机制中的多因素:文献综述
Miriam Basta, Christian Guindi, Sherry Erian
Introduction: Inflammatory Bowel Disease (IBD) is characterized by chronic inflammation in the gastrointestinal tract (GIT) via dysbiosis of the gut microbiome and weakening of the epithelial and mucosal barriers. Although the causative nature of IBD remains unknown, several studies have demonstrated that aberrant host-microRNA (miRNA) activity contributes to its pathophysiology. For example, miRNA-21 contributes to IBD through three mechanisms. Firstly, by increasing gut permeability via the ARF4 pathway. Secondly, by decreasing gut mucosal secretions via interfering with host goblet cells. Finally, by regulating proteins that inhibit host autophagy and decreasing immune response via the Phosphatase and Tensin Homolog (PTEN) and Akt pathway. The proposed study aims to answer the following question: how does aberrant expression of miRNA-21 in IBD contribute to the disease? Methods: This review highlights and summarizes relevant studies on the miRNA-21 regulation of key pathways in the pathogenesis of IBD. Searches used electronic databases including PubMed, and Google Scholar for keywords such as “Inflammatory bowel disease” and “miRNA-21” and other additional relevant terms from years 2016 to 2022. Review papers that met our criteria and the relevant papers they referenced, regardless of their publication date, were manually searched for. Figures were made in part using KeyNote and Serveir Medical Art. Discussion: Intracellular pathways contribute to chronic inflammation in IBD such as the PTEN pathway and pro-inflammatory cytokines like TNF-α. These pathways have been shown to influence the mucosal barrier, epithelial barrier, and the immune system in the gut. These pathways are regulated by miRNA-21, demonstrating miRNA-21 as a key regulator in IBD. Both PTEN and TNF-α also contribute to levels of angiogenesis in the gut through the regulation of vascular endothelial growth factor (VEGF) and hypoxia-inducible factor (HIF), further demonstrating the intricacies of the miRNA-21 pathway regulation in IBD. Conclusion: The research highlighted in this review provides insight into the mechanisms of aberrant miRNA expression in IBD. Furthermore, knowledge of such molecular mechanisms has clinical and research applications, including identifying diagnostic biomarkers, less invasive screening techniques, and novel drug therapies.
简介:炎症性肠病(IBD)以胃肠道(GIT)慢性炎症为特征,通过肠道微生物群失调和上皮和粘膜屏障减弱。尽管IBD的致病性质尚不清楚,但一些研究表明,异常的宿主microrna (miRNA)活性有助于IBD的病理生理。例如,miRNA-21通过三种机制促进IBD。首先,通过ARF4途径增加肠道通透性。其次,通过干扰宿主杯状细胞减少肠道黏膜分泌物。最后,通过Phosphatase and Tensin Homolog (PTEN)和Akt通路调节抑制宿主自噬和降低免疫反应的蛋白。拟议的研究旨在回答以下问题:miRNA-21在IBD中的异常表达如何导致该疾病?方法:本文重点综述了miRNA-21调控IBD发病关键通路的相关研究。使用PubMed和Google Scholar等电子数据库搜索2016年至2022年的“炎症性肠病”和“miRNA-21”等关键词以及其他相关术语。符合我们标准的综述论文及其引用的相关论文,无论其发表日期如何,都是手工检索的。人物部分使用KeyNote和serir医学艺术制作。讨论:细胞内通路有助于IBD的慢性炎症,如PTEN通路和促炎细胞因子如TNF-α。这些途径已被证明影响肠道粘膜屏障、上皮屏障和免疫系统。这些通路受miRNA-21调控,表明miRNA-21是IBD的关键调控因子。PTEN和TNF-α也通过调节血管内皮生长因子(VEGF)和缺氧诱导因子(HIF)来促进肠道血管生成水平,进一步证明了miRNA-21通路在IBD中调控的复杂性。结论:本综述重点研究了IBD中miRNA异常表达的机制。此外,这种分子机制的知识具有临床和研究应用,包括识别诊断性生物标志物,低侵入性筛选技术和新型药物治疗。
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引用次数: 0
Dr. Richard E. Peter 2023 Biology Conference: Abstract Book Richard E. Peter博士2023生物学会议:摘要书
M. Bobinski, Leah Jackson, Aaron Boyd, Jiahui Wang
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引用次数: 0
Factors that Impact Patient Satisfaction and Perceptions in Patient-Physician Interactions in Canada: A Literature Review 加拿大医患互动中影响患者满意度和感知的因素:文献综述
Marwa Aoude
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引用次数: 0
Decolonizing Water Discussions: A Look at the Indigenous Water Crisis in Canada from an Anti-Settler Colonialist Perspective 非殖民化的水讨论:从反移民殖民主义的角度看加拿大原住民的水危机
Brian Ragsdale, Mark Shew
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引用次数: 0
WISE National Conference 2023: Leaders of Tomorrow WISE全国会议2023:明天的领导者
Suzanne M. Wong, Sarvnaz Ale Mohammad, Isabella Wong, Wanda W Janaeska
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引用次数: 0
WISE National Conference 2023: Leaders of Tomorrow WISE全国会议2023:明天的领导者
Suzanne M. Wong, Sarvnaz Ale Mohammad, Isabella Wong, Wanda W. Janaeska
Our goal at Women in Science and Engineering – University of Toronto Chapter is to support and empower all women in STEM fields and to help them achieve their full potential as future engineers, entrepreneurs, scientists, and leaders. Since its inception in 1999, the organization has developed into one of the largest and highly regarded campus organizations with over 1500 members to champion gender equity, counter biases, and build confidence in all STEM fields. Our annual National Conference aims to empower and inspire individuals to pursue their passions, explore new opportunities, and to make meaningful, lasting connections. One of the events we hold at the conference is the 3 Minute Thesis (3MT) competition, which challenges undergraduate and graduate delegates to present their research in three minutes with one static slide to a non-specialist audience. This abstract book features the research that some of the 3MT competitors presented at the WISE National Conference 2023.
我们在科学与工程女性-多伦多大学分会的目标是支持和赋予STEM领域的所有女性权力,帮助她们充分发挥潜力,成为未来的工程师、企业家、科学家和领导者。自1999年成立以来,该组织已发展成为规模最大、备受推崇的校园组织之一,拥有1500多名成员,致力于倡导性别平等、反对偏见,并在所有STEM领域建立信心。我们的年度全国会议旨在授权和激励个人追求他们的激情,探索新的机会,并建立有意义的,持久的联系。我们在会议上举办的活动之一是3分钟论文(3MT)竞赛,该竞赛要求本科生和研究生代表在三分钟内用一张静态幻灯片向非专业观众展示他们的研究。这本抽象的书的特点是一些3MT竞争对手在2023年WISE全国会议上提出的研究。
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引用次数: 0
Celiac Disease and a Gluten-Free Diet Lead to Loss of Methanobrevibacter from the Gut Microbiome 乳糜泻和无麸质饮食导致肠道微生物群中甲烷预防菌的损失
Clayton Rawson, Victoria Hooper, Riley Hansen, Michaela A. Gazdik Stofer
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引用次数: 0
Bench2Bedside 2022 Case Competition & Conference: Translational Research Proposals Bench2Bedside 2022案例竞赛与会议:转化研究提案
Rvaha Afaan, Deepthi Thommandram, Aljeena R Qureshi, Devan Desai
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引用次数: 0
Feasibility Study: Machine Learning in Neurodegenerative Disorders, Alzheimer’s Disease 可行性研究:神经退行性疾病、阿尔茨海默病的机器学习
Xiangxuan Kong
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引用次数: 0
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Undergraduate Research in Natural and Clinical Science and Technology (URNCST) Journal
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