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本文引用的文献

1
YAP induces a neonatal-like pro-renewal niche in the adult heart.YAP在成体心脏中诱导出一种类似新生儿的促再生微环境。
Nat Cardiovasc Res. 2024 Mar;3(3):283-300. doi: 10.1038/s44161-024-00428-w. Epub 2024 Feb 14.
2
Heart regeneration: 20 years of progress and renewed optimism.心脏再生:20 年的进展与重燃的乐观。
Dev Cell. 2022 Feb 28;57(4):424-439. doi: 10.1016/j.devcel.2022.01.012.
3
Yap Promotes Noncanonical Wnt Signals From Cardiomyocytes for Heart Regeneration. Yap 通过促进心肌细胞的非经典 wnt 信号促进心脏再生。
Circ Res. 2021 Oct;129(8):782-797. doi: 10.1161/CIRCRESAHA.121.318966. Epub 2021 Aug 23.
4
YAP Partially Reprograms Chromatin Accessibility to Directly Induce Adult Cardiogenesis In Vivo.YAP 部分重编程染色质可及性以直接在体内诱导成人心肌发生。
Dev Cell. 2019 Mar 25;48(6):765-779.e7. doi: 10.1016/j.devcel.2019.01.017. Epub 2019 Feb 14.
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Complement Receptor C5aR1 Plays an Evolutionarily Conserved Role in Successful Cardiac Regeneration.补体受体 C5aR1 在成功的心脏再生中发挥着进化保守的作用。
Circulation. 2018 May 15;137(20):2152-2165. doi: 10.1161/CIRCULATIONAHA.117.030801. Epub 2018 Jan 18.
6
Actin cytoskeletal remodeling with protrusion formation is essential for heart regeneration in Hippo-deficient mice.肌动蛋白细胞骨架重塑与突起形成对缺失Hippo基因的小鼠心脏再生至关重要。
Sci Signal. 2015 May 5;8(375):ra41. doi: 10.1126/scisignal.2005781.
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Regulation of insulin-like growth factor signaling by Yap governs cardiomyocyte proliferation and embryonic heart size.Yap 通过调节胰岛素样生长因子信号来控制心肌细胞的增殖和胚胎心脏的大小。
Sci Signal. 2011 Oct 25;4(196):ra70. doi: 10.1126/scisignal.2002278.
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Transient regenerative potential of the neonatal mouse heart.新生鼠心脏的短暂再生潜能。
Science. 2011 Feb 25;331(6020):1078-80. doi: 10.1126/science.1200708.
9
Zebrafish heart regeneration occurs by cardiomyocyte dedifferentiation and proliferation.斑马鱼的心脏再生是通过心肌细胞去分化和增殖来实现的。
Nature. 2010 Mar 25;464(7288):606-9. doi: 10.1038/nature08899.
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Primary contribution to zebrafish heart regeneration by gata4(+) cardiomyocytes.Gata4(+) 心肌细胞对斑马鱼心脏再生的主要贡献。
Nature. 2010 Mar 25;464(7288):601-5. doi: 10.1038/nature08804.

一种将心脏微环境与再生联系起来的细胞三联体。

A cellular triad for linking cardiac niche to regeneration.

作者信息

Ma Xiaokai, Hou Junjie, Xiong Jing-Wei

机构信息

Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Institute of Molecular Medicine, and College of Future Technology, Peking University, Beijing, 100871, China.

School of Basic Medical Sciences, Institute of Biomedical Innovation, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, 330031, China.

出版信息

Cell Regen. 2024 Dec 10;13(1):29. doi: 10.1186/s13619-024-00213-x.

DOI:10.1186/s13619-024-00213-x
PMID:39653982
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11628456/
Abstract

Cardiovascular disease is the leading cause of mortality with very limited therapeutic interventions, thus holding great hope for cardiac regenerative medicine. A recent work from Martin's laboratory reports their identification of a fetal-like cardiomyocyte progenitor, adult cardiomyocyte type 2 (aCM2), and its potential interactions with C3 cardiac fibroblasts and C3ar1 macrophages to form a regenerative cellular triad, which is only present in the regenerative heart models, YAP5SA-expressing adult hearts and neonatal hearts. The complement signaling is essential for cellular interactions in this regenerative triad. This Highlight summarizes these major findings and provides brief perspectives on the impact of this regenerative niche during cardiac regeneration in the future.

摘要

心血管疾病是导致死亡的主要原因,而治疗干预非常有限,因此心脏再生医学寄予了厚望。马丁实验室最近的一项研究报告称,他们鉴定出一种胎儿样心肌细胞祖细胞,即成年心肌细胞2型(aCM2),以及它与C3心脏成纤维细胞和C3ar1巨噬细胞之间潜在的相互作用,从而形成一个再生细胞三联体,该三联体仅存在于再生心脏模型、表达YAP5SA的成年心脏和新生心脏中。补体信号对于这个再生三联体中的细胞相互作用至关重要。本综述总结了这些主要发现,并简要展望了这个再生生态位在未来心脏再生过程中的影响。