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心肌细胞中的肾母细胞瘤抑制因子WT1:对心脏稳态和修复的影响

The Wilms' Tumor Suppressor WT1 in Cardiomyocytes: Implications for Cardiac Homeostasis and Repair.

作者信息

Díaz Del Moral Sandra, Wagner Nicole, Wagner Kay-Dietrich

机构信息

Université Côte d'Azur, CNRS, INSERM, iBV, 06107 Nice, France.

出版信息

Cells. 2024 Dec 17;13(24):2078. doi: 10.3390/cells13242078.

DOI:10.3390/cells13242078
PMID:39768169
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11674098/
Abstract

The Wilms' tumor suppressor WT1 is essential for the development of the heart, among other organs such as the kidneys and gonads. The Wt1 gene encodes a zinc finger transcription factor that regulates proliferation, cellular differentiation processes, and apoptosis. WT1 is also involved in cardiac homeostasis and repair. In adulthood, WT1-expression levels are lower compared to those observed through development, and WT1 expression is restricted to a few cell types. However, its systemic deletion in adult mice is lethal, demonstrating that its presence is also key for organ maintenance. In response to injury, the epicardium re-activates the expression of WT1, but little is known about the roles it plays in cardiomyocytes, which are the main cell type affected after myocardial infarction. The fact that cardiomyocytes exhibit a low proliferation rate in the adult heart in mammals highlights the need to explore new approaches for cardiac regeneration. The aim of this review is to emphasize the functions carried out by WT1 in cardiomyocytes in cardiac homeostasis and heart regeneration.

摘要

肾母细胞瘤抑癌基因WT1对心脏以及肾脏和性腺等其他器官的发育至关重要。Wt1基因编码一种锌指转录因子,该因子调节细胞增殖、细胞分化过程和细胞凋亡。WT1还参与心脏内环境稳定和修复。在成年期,与发育过程中观察到的水平相比,WT1的表达水平较低,且WT1的表达仅限于少数细胞类型。然而,在成年小鼠中全身敲除WT1是致命的,这表明它的存在对器官维持也很关键。在受到损伤时,心外膜会重新激活WT1的表达,但对于它在心肌细胞(心肌梗死后受影响的主要细胞类型)中所起的作用知之甚少。哺乳动物成年心脏中心肌细胞增殖率较低这一事实凸显了探索心脏再生新方法的必要性。本综述的目的是强调WT1在心肌细胞的心脏内环境稳定和心脏再生中所发挥的功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0361/11674098/66f50dd0567a/cells-13-02078-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0361/11674098/9e0c67bc5b99/cells-13-02078-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0361/11674098/e21b311a7ac1/cells-13-02078-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0361/11674098/8d3670cf8aed/cells-13-02078-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0361/11674098/1cec48efb53e/cells-13-02078-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0361/11674098/66f50dd0567a/cells-13-02078-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0361/11674098/9e0c67bc5b99/cells-13-02078-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0361/11674098/e21b311a7ac1/cells-13-02078-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0361/11674098/8d3670cf8aed/cells-13-02078-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0361/11674098/1cec48efb53e/cells-13-02078-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0361/11674098/66f50dd0567a/cells-13-02078-g005.jpg

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