There are critical molecular mechanisms that can be activated to induce myocardial repair, and in humans this is most efficient during fetal development. The timing of heart development in relation to birth and the size/electrophysiology of the heart are similar in humans and sheep, providing a model to investigate the repair capacity of the mammalian heart and how this can be applied to adult heart repair. Myocardial infarction was induced by ligation of the left anterior descending coronary artery in fetal (105 days gestation when cardiomyocytes are proliferative) and adolescent sheep (6 mo of age when all cardiomyocytes have switched to an adult phenotype). An ovine gene microarray was used to compare gene expression in sham and infarcted (remote, border and infarct areas) cardiac tissue from fetal and adolescent hearts. The gene response to myocardial infarction was less pronounced in fetal compared with adolescent sheep hearts and there were unique gene responses at each age. There were also region-specific changes in gene expression between each age, in the infarct tissue, tissue bordering the infarct, and tissue remote from the infarction. In total, there were 880 genes that responded to MI uniquely in the adolescent samples compared with 170 genes in the fetal response, as well as 742 overlap genes that showed concordant direction of change responses to infarction at both ages. In response to myocardial infarction, there were specific changes in genes within pathways of mitochondrial oxidation, muscle contraction, and hematopoietic cell lineages, suggesting that the control of energy utilization and immune function are critical for effective heart repair. The more restricted gene response in the fetus may be an important factor in its enhanced capacity for cardiac repair.

中文翻译：

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胎儿和青春期绵羊心脏梗塞后三天的差异基因反应。

有一些关键的分子机制可以被激活以诱导心肌修复，而在人类中，这在胎儿发育过程中是最有效的。在人和羊中，与出生有关的心脏发育时机以及心脏的大小/电生理学相似，为研究哺乳动物心脏的修复能力以及如何将其应用于成人心脏修复提供了模型。结扎胎儿（当心肌细胞增生时，妊娠105天）和青春期的绵羊（所有心肌细胞均已转变为成年表型，年龄为6 mo）时，左前降支冠状动脉结扎可诱发心肌梗塞。使用绵羊基因微阵列比较假胎和胎儿和青少年心脏梗死（远端，边界和梗死区域）心脏组织中的基因表达。与青春期绵羊心脏相比，胎儿对心肌梗塞的基因反应较不明显，并且在每个年龄段都有独特的基因反应。在每个年龄之间，在梗塞组织中，与梗塞接壤的组织和远离梗塞的组织之间，基因表达也存在区域特定的变化。总计，在青春期样本中有880个基因对MI产生独特的反应，而在胎儿反应中只有170个基因，还有742个重叠基因在两个年龄段均显示出对梗死变化反应一致的方向。在应对心肌梗塞时，线粒体氧化，肌肉收缩和造血细胞谱系通路中的基因发生了特定变化，这表明能量利用和免疫功能的控制对于有效的心脏修复至关重要。