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蝾螈肢体再生过程中的假定上皮-间充质转化:当前观点和未来研究。

Putative epithelial-mesenchymal transitions during salamander limb regeneration: Current perspectives and future investigations.

机构信息

Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, Massachusetts, USA.

Broad Institute of Harvard and MIT, Cambridge, Massachusetts, USA.

出版信息

Ann N Y Acad Sci. 2024 Oct;1540(1):89-103. doi: 10.1111/nyas.15210. Epub 2024 Sep 13.

DOI:10.1111/nyas.15210
PMID:39269330
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11471381/
Abstract

Previous studies have implicated epithelial-mesenchymal transition (EMT) in salamander limb regeneration. In this review, we describe putative roles for EMT during each stage of limb regeneration in axolotls and other salamanders. We hypothesize that EMT and EMT-like gene expression programs may regulate three main cellular processes during limb regeneration: (1) keratinocyte migration during wound closure; (2) transient invasion of the stump by epithelial cells undergoing EMT; and (3) use of EMT-like programs by non-epithelial blastemal progenitor cells to escape the confines of their niches. Finally, we propose nontraditional roles for EMT during limb regeneration that warrant further investigation, including alternative EMT regulators, stem cell activation, and fibrosis induced by aberrant EMT.

摘要

先前的研究表明上皮-间充质转化(EMT)在蝾螈肢体再生中起作用。在这篇综述中,我们描述了 EMT 在蝾螈和其他蝾螈肢体再生的每个阶段中的可能作用。我们假设 EMT 和 EMT 样基因表达程序可能调节肢体再生过程中的三个主要细胞过程:(1)伤口闭合过程中角质形成细胞的迁移;(2) EMT 上皮细胞对残肢的短暂侵袭;(3)非上皮性芽基细胞利用 EMT 样程序逃避其龛位的限制。最后,我们提出了 EMT 在肢体再生中的非传统作用,这些作用值得进一步研究,包括 EMT 的替代调节因子、干细胞激活以及 EMT 异常引起的纤维化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ce4/11471381/3abbf3ee32c0/nihms-2015595-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ce4/11471381/92094d9e74fc/nihms-2015595-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ce4/11471381/e30cffb91d08/nihms-2015595-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ce4/11471381/3abbf3ee32c0/nihms-2015595-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ce4/11471381/92094d9e74fc/nihms-2015595-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ce4/11471381/e30cffb91d08/nihms-2015595-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ce4/11471381/3abbf3ee32c0/nihms-2015595-f0004.jpg

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本文引用的文献

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Biol Open. 2024 Feb 15;13(2). doi: 10.1242/bio.060152. Epub 2024 Feb 6.
2
Epithelial-mesenchymal transition: an organizing principle of mammalian regeneration.上皮-间质转化:哺乳动物再生的组织原则
Front Cell Dev Biol. 2023 Oct 26;11:1101480. doi: 10.3389/fcell.2023.1101480. eCollection 2023.
3
miR-33a-3p regulates METTL3-mediated AREG stability and alters EMT to inhibit pancreatic cancer invasion and metastasis.
miR-33a-3p 通过调控 METTL3 介导的 AREG 稳定性改变 EMT 抑制胰腺癌侵袭转移
Sci Rep. 2023 Aug 21;13(1):13587. doi: 10.1038/s41598-023-39506-7.
4
An "unexpected" role for EMT transcription factors in hematological development and malignancy.EMT 转录因子在血液系统发育和恶性肿瘤中的“意外”作用。
Front Immunol. 2023 Aug 3;14:1207360. doi: 10.3389/fimmu.2023.1207360. eCollection 2023.
5
Molecular profile of metastasis, cell plasticity and EMT in pancreatic cancer: a pre-clinical connection to aggressiveness and drug resistance.胰腺癌转移、细胞可塑性和 EMT 的分子特征:临床前侵袭性和耐药性的联系。
Cancer Metastasis Rev. 2024 Mar;43(1):29-53. doi: 10.1007/s10555-023-10125-y. Epub 2023 Jul 15.
6
An ERK-dependent molecular switch antagonizes fibrosis and promotes regeneration in spiny mice ().ERK 依赖性分子开关拮抗纤维化并促进刺鼠的再生 ()。
Sci Adv. 2023 Apr 28;9(17):eadf2331. doi: 10.1126/sciadv.adf2331. Epub 2023 Apr 26.
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