维生素A缺乏可减轻stra6缺陷心脏缺血损伤后的心脏破裂。

IF 2.8 3区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS
Frontiers in Cardiovascular Medicine Pub Date : 2025-09-16 eCollection Date: 2025-01-01 DOI:10.3389/fcvm.2025.1626769
Yannick Smolenski, Natali Froese, Paolo Galuppo, Christopher Werlein, Anna Gigina, Steven R Talbot, Sergej Erschow, Dirk Wedekind, Robert Geffers, Norbert B Ghyselinck, Heike Bähre, Jan C Kamp, Lavinia Neubert, Melanie Ricke-Hoch, Johann Bauersachs, Christian Riehle
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引用次数: 0

摘要

背景:受视黄酸基因6 (STRA6)刺激的细胞表面受体调节维生素a代谢物的细胞摄取和心脏发育。我们假设Stra6表达通过维生素a依赖机制减轻心肌梗死(MI)后缺血性损伤诱导的心力衰竭。方法:采用卵磷脂-视黄醇酰基转移酶(Lrat)联合种系缺失和维生素A缺乏(VitAD)诱导Stra6种系缺失小鼠心肌梗死,并用缺乏维生素A的饮食喂养。通过经胸超声心动图确定收缩功能,通过组织学分析评估心脏结构,并通过RNA测序进行基因谱分析。结果:在基础条件下,Stra6缺失和VitAD对心脏收缩功能和结构没有影响。Stra6缺乏导致心肌破裂,大多数小鼠在心肌梗死后4天死亡,进一步的VitAD减弱。有趣的是,心肌梗死后3天各组之间的收缩功能、心力衰竭标志物mRNA表达和心脏结构没有差异。心肌梗死后3天的基因分析显示,与野生型心脏相比,stra6缺陷心脏的Wnt信号传导减少,VitAD逆转了这一现象。结论:本研究发现了VitAD的一个意想不到的作用,它保留了Wnt信号并减轻了stra6缺陷心脏缺血损伤后的心脏破裂。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Vitamin A deficiency attenuates cardiac rupture in Stra6-deficient hearts following ischemic injury.

Background: Stimulated by retinoic acid gene 6 (STRA6) is a cell surface receptor that regulates cellular uptake of vitamin A metabolites and cardiac development. We hypothesized that Stra6 expression attenuates ischemic injury-induced heart failure following myocardial infarction (MI) by vitamin A-dependent mechanisms.

Methods: MI was induced in mice with Stra6 germline deletion, vitamin A deficiency (VitAD) by combined lecithin-retinol acyltransferase (Lrat) germline deletion and feeding with a vitamin A-deficient diet. Contractile function was determined by transthoracic echocardiography, cardiac structure was assessed by histological analysis, and gene profiling was performed by RNA sequencing.

Results: Stra6 deletion and VitAD did not impact contractile function and cardiac structure under basal conditions. Stra6 deficiency resulted in myocardial rupture, with the majority of mice dying by 4 days post-MI, which additional VitAD attenuated. Interestingly, contractile function, mRNA expression of heart failure markers, and cardiac structure were not different between groups 3 days post-MI. Gene profiling 3 days post-MI revealed decreased Wnt signaling in Stra6-deficient relative to wildtype hearts, which was reversed by VitAD.

Conclusion: The present study identifies an unexpected role for VitAD, which preserves Wnt signaling and attenuates cardiac rupture in Stra6-deficient hearts following ischemic injury.

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来源期刊
Frontiers in Cardiovascular Medicine
Frontiers in Cardiovascular Medicine Medicine-Cardiology and Cardiovascular Medicine
CiteScore
3.80
自引率
11.10%
发文量
3529
审稿时长
14 weeks
期刊介绍: Frontiers? Which frontiers? Where exactly are the frontiers of cardiovascular medicine? And who should be defining these frontiers? At Frontiers in Cardiovascular Medicine we believe it is worth being curious to foresee and explore beyond the current frontiers. In other words, we would like, through the articles published by our community journal Frontiers in Cardiovascular Medicine, to anticipate the future of cardiovascular medicine, and thus better prevent cardiovascular disorders and improve therapeutic options and outcomes of our patients.
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