Stroke can induce cardiac dysfunction in the absence of primary cardiac disease; however, the mechanisms underlying the interaction between the neurological deficits and the heart are poorly understood. The objective of this study was to investigate the effects of stroke on cardiac function and to identify the transcriptome characteristics of the heart. Stroke significantly decreased heart weight/tibia length ratio and cardiomyocyte cross-sectional areas and increased atrogin-1 and the E3 ubiquitin ligase MuRF-1, indicating myocardial atrophy in MCAO-induced mouse hearts. RNA sequencing of mRNA revealed 383 differentially expressed genes (DEGs) in MCAO myocardium, of which 221 were downregulated and 162 upregulated. Grouping of DEGs based on biological function and quantitative PCR validation indicated that suppressed immune response and collagen synthesis and altered activity of oxidoreductase, peptidase, and endopeptidase may be involved in MCAO-induced cardiomyopathy. The DEGs were mainly distributed in the membrane or extracellular region of cardiomyocytes and acted as potential mediators of stroke-induced cardiac dysregulation involved in cardiac atrophy. Stroke induced a unique transcriptome response in the myocardium and resulted in immediate cardiac atrophy and dysfunction.

中文翻译：

---

缺血性中风诱导心脏功能障碍并改变小鼠的转录组谱

在没有原发性心脏病的情况下，中风可诱发心功能不全；然而，人们对神经功能缺损与心脏之间相互作用的潜在机制知之甚少。本研究的目的是研究中风对心脏功能的影响，并确定心脏的转录组特征。中风显着降低心脏重量/胫骨长度比和心肌细胞横截面积，增加 atrogin-1 和 E3 泛素连接酶 MuRF-1，表明 MCAO 诱导的小鼠心脏心肌萎缩。mRNA 的 RNA 测序显示 MCAO 心肌中有 383 个差异表达基因 (DEG)，其中 221 个下调，162 个上调。基于生物学功能和定量 PCR 验证的 DEG 分组表明，抑制免疫反应和胶原蛋白合成以及改变氧化还原酶、肽酶和内肽酶的活性可能与 MCAO 诱导的心肌病有关。DEGs 主要分布在心肌细胞的膜或细胞外区域，是中风诱发的心脏萎缩的潜在介质。中风在心肌中诱导了独特的转录组反应，并导致立即的心脏萎缩和功能障碍。DEGs 主要分布在心肌细胞的膜或细胞外区域，是中风诱导的心脏功能失调参与心脏萎缩的潜在介质。中风在心肌中诱导了独特的转录组反应，并导致立即的心脏萎缩和功能障碍。DEGs 主要分布在心肌细胞的膜或细胞外区域，是中风诱导的心脏功能失调参与心脏萎缩的潜在介质。中风在心肌中诱导了独特的转录组反应，并导致立即的心脏萎缩和功能障碍。