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二十年心脏再生研究:心肌细胞增殖及其他。

Two decades of heart regeneration research: Cardiomyocyte proliferation and beyond.

机构信息

Department of Biological Sciences, San Jose State University, San Jose, California, USA.

Department of Physiology, Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California, USA.

出版信息

WIREs Mech Dis. 2024 Jan-Feb;16(1):e1629. doi: 10.1002/wsbm.1629. Epub 2023 Sep 12.

DOI:10.1002/wsbm.1629
PMID:37700522
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10840678/
Abstract

Interest in vertebrate cardiac regeneration has exploded over the past two decades since the discovery that adult zebrafish are capable of complete heart regeneration, contrasting the limited regenerative potential typically observed in adult mammalian hearts. Undercovering the mechanisms that both support and limit cardiac regeneration across the animal kingdom may provide unique insights in how we may unlock this capacity in adult humans. In this review, we discuss key discoveries in the heart regeneration field over the last 20 years. Initially, seminal findings revealed that pre-existing cardiomyocytes are the major source of regenerated cardiac muscle, drawing interest into the intrinsic mechanisms regulating cardiomyocyte proliferation. Moreover, recent studies have identified the importance of intercellular interactions and physiological adaptations, which highlight the vast complexity of the cardiac regenerative process. Finally, we compare strategies that have been tested to increase the regenerative capacity of the adult mammalian heart. This article is categorized under: Cardiovascular Diseases > Stem Cells and Development.

摘要

在过去的二十年中,人们对脊椎动物心脏再生的兴趣激增,因为人们发现成年斑马鱼具有完全的心脏再生能力,这与成年哺乳动物心脏通常观察到的有限的再生潜力形成了鲜明对比。揭示支持和限制整个动物界心脏再生的机制,可能为我们如何在成年人类中释放这种能力提供独特的见解。在这篇综述中,我们讨论了过去 20 年来心脏再生领域的重要发现。最初的重要发现揭示了预先存在的心肌细胞是再生心肌的主要来源,这引起了人们对调节心肌细胞增殖的内在机制的兴趣。此外,最近的研究还确定了细胞间相互作用和生理适应的重要性,这突显了心脏再生过程的巨大复杂性。最后,我们比较了已被测试用于提高成年哺乳动物心脏再生能力的策略。本文属于以下分类:心血管疾病 > 干细胞和发育。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8da8/10840678/df695bd1e1af/nihms-1928210-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8da8/10840678/9bec3eba6026/nihms-1928210-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8da8/10840678/a078c3f884fc/nihms-1928210-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8da8/10840678/48c02b3ed30c/nihms-1928210-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8da8/10840678/df695bd1e1af/nihms-1928210-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8da8/10840678/9bec3eba6026/nihms-1928210-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8da8/10840678/a078c3f884fc/nihms-1928210-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8da8/10840678/48c02b3ed30c/nihms-1928210-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8da8/10840678/df695bd1e1af/nihms-1928210-f0005.jpg

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J Mol Cell Cardiol. 2023 Apr;177:9-20. doi: 10.1016/j.yjmcc.2023.02.002. Epub 2023 Feb 17.
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Systemic Hypoxemia Induces Cardiomyocyte Hypertrophy and Right Ventricular Specific Induction of Proliferation.
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