• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

通过组学技术揭示肠道缺血再灌注损伤的分子复杂性。

Unveiling the molecular complexity of intestinal ischemia-reperfusion injury through omics technologies.

机构信息

Department of Surgery, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, The Netherlands.

出版信息

Proteomics. 2024 Jun;24(12-13):e2300160. doi: 10.1002/pmic.202300160. Epub 2024 Mar 13.

DOI:10.1002/pmic.202300160
PMID:38477684
Abstract

Intestinal ischemia-reperfusion injury (IR) is implicated in various clinical conditions and causes damage to the intestinal epithelium resulting in intestinal barrier loss. This presents a substantial clinical challenge, emphasizing the importance of gaining a comprehensive understanding of molecular events to aid in the identification of novel therapeutic targets. This review systematically explores the extent to which omics technologies-transcriptomics, proteomics, metabolomics, and metagenomics-have already contributed to deciphering the molecular mechanisms contributing to intestinal IR injury, in in vivo and in vitro animal and human models, and in clinical samples. Recent breakthroughs involve applying omics methodologies on exosomes, organoids, and single cells, shedding light on promising avenues and valuable targets to reduce intestinal IR injury. Future directions aimed at expediting clinical translation are discussed as well and include multi-omics data integration to facilitate the identification of key regulatory nodes driving intestinal IR injury and advancing human organoid models based on the novel insights by single-cell omics technologies, offering hope for clinical application of therapeutic strategies in the years to come.

摘要

肠缺血再灌注损伤(IR)与多种临床情况有关,可导致肠上皮损伤,进而使肠道屏障丧失。这是一个重大的临床挑战,强调了全面了解分子事件的重要性,以帮助确定新的治疗靶点。本综述系统地探讨了组学技术(转录组学、蛋白质组学、代谢组学和宏基因组学)在多大程度上有助于解析参与肠 IR 损伤的分子机制,包括在体内和体外动物和人类模型以及临床样本中的作用。最近的突破涉及在细胞外囊泡、类器官和单细胞上应用组学方法,为减少肠 IR 损伤提供了有前途的途径和有价值的靶点。本文还讨论了旨在加速临床转化的未来方向,包括多组学数据的整合,以促进识别关键调控节点,推动基于单细胞组学技术的新型人类类器官模型的发展,为未来治疗策略的临床应用带来希望。

相似文献

1
Unveiling the molecular complexity of intestinal ischemia-reperfusion injury through omics technologies.通过组学技术揭示肠道缺血再灌注损伤的分子复杂性。
Proteomics. 2024 Jun;24(12-13):e2300160. doi: 10.1002/pmic.202300160. Epub 2024 Mar 13.
2
Proteomics analysis of human intestinal organoids during hypoxia and reoxygenation as a model to study ischemia-reperfusion injury.缺氧和复氧期间人肠类器官的蛋白质组学分析作为研究缺血再灌注损伤的模型。
Cell Death Dis. 2021 Jan 18;12(1):95. doi: 10.1038/s41419-020-03379-9.
3
Human breast milk-derived exosomes protect against intestinal ischemia and reperfusion injury in neonatal rats.人乳来源的外泌体可预防新生大鼠肠缺血再灌注损伤。
J Pediatr Surg. 2022 Jul;57(7):1264-1268. doi: 10.1016/j.jpedsurg.2022.02.029. Epub 2022 Mar 13.
4
Temporal Transcript Profiling Identifies a Role for Unfolded Protein Stress in Human Gut Ischemia-Reperfusion Injury.时间转录谱分析鉴定未折叠蛋白应激在人类肠道缺血再灌注损伤中的作用。
Cell Mol Gastroenterol Hepatol. 2022;13(3):681-694. doi: 10.1016/j.jcmgh.2021.11.001. Epub 2021 Nov 11.
5
The Potential Role of Protein Tyrosine Phosphatase, Receptor Type C (CD45) in the Intestinal Ischemia-Reperfusion Injury.蛋白酪氨酸磷酸酶C型受体(CD45)在肠道缺血再灌注损伤中的潜在作用
J Comput Biol. 2020 Aug;27(8):1303-1312. doi: 10.1089/cmb.2019.0244. Epub 2019 Dec 20.
6
Rapid reversal of human intestinal ischemia-reperfusion induced damage by shedding of injured enterocytes and reepithelialisation.通过受损肠上皮细胞脱落和重新上皮化快速逆转人类肠道缺血再灌注诱导的损伤。
PLoS One. 2008;3(10):e3428. doi: 10.1371/journal.pone.0003428. Epub 2008 Oct 17.
7
Animal models of ischemia-reperfusion-induced intestinal injury: progress and promise for translational research.缺血再灌注诱导肠损伤的动物模型:转化研究的进展与前景。
Am J Physiol Gastrointest Liver Physiol. 2015 Jan 15;308(2):G63-75. doi: 10.1152/ajpgi.00112.2013. Epub 2014 Nov 20.
8
Effect of N-Acetylserotonin on Intestinal Recovery Following Intestinal Ischemia-Reperfusion Injury in a Rat.N-乙酰血清素对大鼠肠缺血再灌注损伤后肠恢复的影响
Eur J Pediatr Surg. 2016 Feb;26(1):47-53. doi: 10.1055/s-0035-1559886. Epub 2015 Sep 17.
9
TLR2 modulates antibodies required for intestinal ischemia/reperfusion-induced damage and inflammation.Toll样受体2(TLR2)调节肠道缺血/再灌注诱导的损伤和炎症所需的抗体。
J Immunol. 2015 Feb 1;194(3):1190-8. doi: 10.4049/jimmunol.1303124. Epub 2014 Dec 24.
10
HIF-1 mediates pathogenic inflammatory responses to intestinal ischemia-reperfusion injury.低氧诱导因子-1 介导肠道缺血再灌注损伤的致病炎症反应。
Am J Physiol Gastrointest Liver Physiol. 2010 Oct;299(4):G833-43. doi: 10.1152/ajpgi.00065.2010. Epub 2010 Aug 5.

引用本文的文献

1
Mitochondrial alanyl-tRNA synthetase 2 mediates histone lactylation to promote ferroptosis in intestinal ischemia-reperfusion injury.线粒体丙氨酰-tRNA合成酶2介导组蛋白乳酰化以促进肠道缺血再灌注损伤中的铁死亡。
World J Gastrointest Surg. 2025 Jun 27;17(6):106777. doi: 10.4240/wjgs.v17.i6.106777.
2
Proteomic analysis of human kidney biopsies unveils emerging acute kidney injury very early after liver graft reperfusion.对人类肾活检组织进行蛋白质组学分析发现,肝移植再灌注后极早期就出现了新发急性肾损伤。
J Transl Med. 2025 Jun 16;23(1):658. doi: 10.1186/s12967-025-06695-w.
3
Bifidobacterium longum Metabolite Indole-3-Carboxaldehyde Blocks HDAC3 and Inhibits Macrophage NLRP3 Inflammasome Activation in Intestinal Ischemia/Reperfusion Injury.
长双歧杆菌代谢产物吲哚 - 3 - 甲醛可阻断HDAC3并抑制肠道缺血/再灌注损伤中巨噬细胞NLRP3炎性小体的激活。
Inflammation. 2024 Dec 11. doi: 10.1007/s10753-024-02211-2.