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生长分化因子11(GDF-11)缺乏通过损害心脏血管生成加速压力超负荷诱导的心力衰竭。

Deficiency of GDF-11 Accelerates TAC-Induced Heart Failure by Impairing Cardiac Angiogenesis.

作者信息

Zhu Jinyun, Zhang Ning, Zhao Yun, Liu Qi, Wang Yingchao, Chen Mingyao, Ma Qunchao, Dong Aiqiang, Wang Yaping, Yu Hong

机构信息

Department of Cardiology, Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.

Cardiovascular Key Laboratory of Zhejiang Province, Hangzhou, China.

出版信息

JACC Basic Transl Sci. 2023 Feb 22;8(6):617-635. doi: 10.1016/j.jacbts.2022.11.004. eCollection 2023 Jun.

DOI:10.1016/j.jacbts.2022.11.004
PMID:37426531
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10322730/
Abstract

The role of growth differentiation factor (GDF)-11 in cardiac diseases has not been fully determined. Our study revealed that GDF-11 is not essential for myocardial development and physiological growth, whereas its absence exacerbates heart failure under pressure overload condition via impairing the responsive angiogenesis. GDF-11 induced VEGF expression in CMs by activating the Akt/mTOR pathway. The effect of endogenous GDF-11 on the heart belongs to local self-regulation of myocardial tissue, rather than a way of systemic regulation.

摘要

生长分化因子(GDF)-11在心脏疾病中的作用尚未完全明确。我们的研究表明,GDF-11对心肌发育和生理性生长并非必不可少,然而,在压力超负荷情况下,其缺失会通过损害反应性血管生成而加剧心力衰竭。GDF-11通过激活Akt/mTOR途径诱导心肌细胞中血管内皮生长因子(VEGF)的表达。内源性GDF-11对心脏的作用属于心肌组织的局部自我调节,而非一种全身调节方式。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66ba/10322730/7d2f657a38b2/gr7.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66ba/10322730/7f97b4889b50/gr1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66ba/10322730/7d2f657a38b2/gr7.jpg

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Oncogenesis. 2021 Jan 8;10(1):1. doi: 10.1038/s41389-020-00288-6.
2
GDF11 inhibits cardiomyocyte pyroptosis and exerts cardioprotection in acute myocardial infarction mice by upregulation of transcription factor HOXA3.GDF11 通过上调转录因子 HOXA3 抑制心肌细胞焦亡并发挥急性心肌梗死小鼠的心脏保护作用。
Cell Death Dis. 2020 Oct 25;11(10):917. doi: 10.1038/s41419-020-03120-6.
3
Candidate rejuvenating factor GDF11 and tissue fibrosis: friend or foe?
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Geroscience. 2020 Dec;42(6):1475-1498. doi: 10.1007/s11357-020-00279-w. Epub 2020 Oct 6.
4
Cardiac Endocrinology: Heart-Derived Hormones in Physiology and Disease.心脏内分泌学:生理与疾病中的心脏源激素
JACC Basic Transl Sci. 2020 Sep 28;5(9):949-960. doi: 10.1016/j.jacbts.2020.05.007. eCollection 2020 Sep.
5
Growth differentiation factor 11 promotes differentiation of MSCs into endothelial-like cells for angiogenesis.生长分化因子 11 可促进间充质干细胞向血管内皮样细胞分化,促进血管生成。
J Cell Mol Med. 2020 Aug;24(15):8703-8717. doi: 10.1111/jcmm.15502. Epub 2020 Jun 25.
6
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Am J Physiol Heart Circ Physiol. 2019 Jul 1;317(1):H201-H212. doi: 10.1152/ajpheart.00615.2018. Epub 2019 May 24.
7
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