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炎症性肠病和结直肠癌发生中肠道干细胞的营养基因组学基础

Nutrigenomic underpinnings of intestinal stem cells in inflammatory bowel disease and colorectal cancer development.

作者信息

Ho Jennifer, Puoplo Nicholas, Pokharel Namrata, Hirdaramani Aanya, Hanyaloglu Aylin C, Cheng Chia-Wei

机构信息

Institute of Human Nutrition, Columbia University Irving Medical Center, New York City, NY, United States.

Columbia Stem Cell Initiative, Columbia University Irving Medical Center, New York City, NY, United States.

出版信息

Front Genet. 2024 Aug 30;15:1349717. doi: 10.3389/fgene.2024.1349717. eCollection 2024.

DOI:10.3389/fgene.2024.1349717
PMID:39280096
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11393785/
Abstract

Food-gene interaction has been identified as a leading risk factor for inflammatory bowel disease (IBD) and colorectal cancer (CRC). Accordingly, nutrigenomics emerges as a new approach to identify biomarkers and therapeutic targets for these two strongly associated gastrointestinal diseases. Recent studies in stem cell biology have further shown that diet and nutrition signal to intestinal stem cells (ISC) by altering nutrient-sensing transcriptional activities, thereby influencing barrier integrity and susceptibility to inflammation and tumorigenesis. This review recognizes the dietary factors related to both CRC and IBD and investigates their impact on the overlapping transcription factors governing stem cell activities in homeostasis and post-injury responses. Our objective is to provide a framework to study the food-gene regulatory network of disease-contributing cells and inspire new nutrigenomic approaches for detecting and treating diet-related IBD and CRC.

摘要

食物-基因相互作用已被确定为炎症性肠病(IBD)和结直肠癌(CRC)的主要危险因素。因此,营养基因组学作为一种新方法出现,用于识别这两种密切相关的胃肠道疾病的生物标志物和治疗靶点。干细胞生物学的最新研究进一步表明,饮食和营养通过改变营养感应转录活性向肠道干细胞(ISC)发出信号,从而影响屏障完整性以及对炎症和肿瘤发生的易感性。本综述识别了与CRC和IBD相关的饮食因素,并研究了它们对在体内平衡和损伤后反应中控制干细胞活动的重叠转录因子的影响。我们的目标是提供一个框架,以研究促成疾病的细胞的食物-基因调控网络,并激发新的营养基因组学方法来检测和治疗与饮食相关的IBD和CRC。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d6d/11393785/40bf79b8f9e9/fgene-15-1349717-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d6d/11393785/1430b605df58/fgene-15-1349717-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d6d/11393785/6f1441c43697/fgene-15-1349717-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d6d/11393785/42efd599593a/fgene-15-1349717-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d6d/11393785/40bf79b8f9e9/fgene-15-1349717-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d6d/11393785/1430b605df58/fgene-15-1349717-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d6d/11393785/6f1441c43697/fgene-15-1349717-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d6d/11393785/42efd599593a/fgene-15-1349717-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d6d/11393785/40bf79b8f9e9/fgene-15-1349717-g004.jpg

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