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细胞可塑性在胃及其他部位的再生中。

Cell plasticity in regeneration in the stomach and beyond.

机构信息

Section of Gastroenterology and Hepatology, Department of Medicine, Baylor College of Medicine, USA. Electronic address: https://twitter.com/@madkinsthreats.

Section of Gastroenterology and Hepatology, Department of Medicine, Baylor College of Medicine, USA; Department of Pathology & Immunology, Baylor College of Medicine, USA; Department of Molecular and Cellular Biology, Baylor College of Medicine, USA.

出版信息

Curr Opin Genet Dev. 2022 Aug;75:101948. doi: 10.1016/j.gde.2022.101948. Epub 2022 Jul 6.

DOI:10.1016/j.gde.2022.101948
PMID:35809361
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10378711/
Abstract

Recent studies using cell lineage-tracing techniques, organoids, and single-cell RNA sequencing analyses have revealed: 1) adult organs use cell plasticity programs to recruit progenitor cells to regenerate tissues after injury, and 2) plasticity is far more common than previously thought, even in homeostasis. Here, we focus on the complex interplay of normal stem cell differentiation and plasticity in homeostasis and after injury, using the gastric epithelium as a touchstone. We also examine common features of regenerative programs and discuss the evolutionarily conserved, stepwise process of paligenosis which reprograms mature cells into progenitors that can repair damaged tissue. Finally, we discuss how conserved plasticity programs may help us better understand pathological processes like metaplasia.

摘要

最近使用细胞谱系追踪技术、类器官和单细胞 RNA 测序分析的研究揭示:1)成年器官利用细胞可塑性程序在损伤后招募祖细胞来再生组织,2)可塑性比以前认为的要普遍得多,即使在体内平衡中也是如此。在这里,我们关注的是胃上皮作为试金石的体内平衡和损伤后正常干细胞分化和可塑性的复杂相互作用。我们还研究了再生程序的共同特征,并讨论了后生作用的进化保守、逐步过程,该过程将成熟细胞重新编程为可以修复受损组织的祖细胞。最后,我们讨论了保守的可塑性程序如何帮助我们更好地理解化生等病理过程。

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2
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本文引用的文献

1
BMP feed-forward loop promotes terminal differentiation in gastric glands and is interrupted by H. pylori-driven inflammation.BMP 前馈回路促进胃腺的终末分化,并被 H. pylori 驱动的炎症所阻断。
Nat Commun. 2022 Mar 24;13(1):1577. doi: 10.1038/s41467-022-29176-w.
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MicroRNA Roles in Cell Reprogramming Mechanisms.MicroRNA 在细胞重编程机制中的作用。
Cells. 2022 Mar 10;11(6):940. doi: 10.3390/cells11060940.
3
Gastric metaplasia could initiate the serrated neoplasia pathway in CRC.胃化生可能启动结直肠癌中的锯齿状肿瘤发生途径。
Nat Rev Gastroenterol Hepatol. 2022 Apr;19(4):217-218. doi: 10.1038/s41575-022-00592-z.
4
Regulation of the double-stranded RNA response through ADAR1 licenses metaplastic reprogramming in gastric epithelium.通过 ADAR1 对双链 RNA 反应的调节,在胃上皮中许可了化生重编程。
JCI Insight. 2022 Feb 8;7(3):e153511. doi: 10.1172/jci.insight.153511.
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Clonal Transitions and Phenotypic Evolution in Barrett's Esophagus.巴雷特食管中的克隆转换和表型演化。
Gastroenterology. 2022 Apr;162(4):1197-1209.e13. doi: 10.1053/j.gastro.2021.12.271. Epub 2021 Dec 29.
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Differential pre-malignant programs and microenvironment chart distinct paths to malignancy in human colorectal polyps.不同的癌前病变程序和微环境描绘了人类结直肠息肉恶变的不同途径。
Cell. 2021 Dec 22;184(26):6262-6280.e26. doi: 10.1016/j.cell.2021.11.031. Epub 2021 Dec 14.
7
ELAPOR1 is a secretory granule maturation-promoting factor that is lost during paligenosis.ELAPOR1 是一种促进分泌颗粒成熟的因子,在衰老过程中会丢失。
Am J Physiol Gastrointest Liver Physiol. 2022 Jan 1;322(1):G49-G65. doi: 10.1152/ajpgi.00246.2021. Epub 2021 Nov 24.
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