Regenerative healing following foetal myocardial infarction.
Regenerative healing following foetal myocardial infarction.
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DOI：
10.1016/j.ejcts.2010.03.049
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发表时间：
2010-12
影响因子：
3.4
通讯作者：
Liechty, Kenneth W.
中科院分区：
文献类型：
--
作者：
Herdrich, Benjamin J.;Danzer, Enrico;Davey, Marcus G.;Allukian, Myron;Englefield, Virginia;Gorman, Joseph H., III;Gorman, Robert C.;Liechty, Kenneth W.
成人对心肌梗死的反应导致炎症、瘢痕形成、左心室扩张以及局部和整体功能的丧失。再生无疤痕愈合已证实在胎儿真皮和肌腱，并与减少炎症。我们假设胎儿心肌梗死后会有最小的炎症，再生愈合和功能保存。在成年或妊娠早期胎羊中产生了占左心室20%的心尖前心肌梗死。采用定量超声心动图连续评估心肌功能。组织学检查梗死结构是否有瘢痕形成的证据。细胞炎症、细胞增殖和细胞凋亡采用免疫组织化学方法进行评估。心肌梗死后4周，成年羊的射血分数明显下降（41±7.4% ~ 26±7.4%,p<0.05），心肌动力段增大（6.9±0.8 cm ~ 7.9±1.1 cm, p<0.05）。相比之下，心肌梗死后4周胎儿射血分数无下降（53±8.1% ~ 55±8.8%），胎儿心肌段无动态变化。与成人相比，胎儿梗死缺乏炎症细胞浸润，愈合时纤维化最小。胎儿梗死也显示BrdU+增殖细胞，包括心肌细胞。这些数据表明，胎儿对心肌梗死的反应与成人有显著不同，其特征是最小的炎症，缺乏纤维化，心肌增殖和心功能恢复。减少炎症与损伤后胎儿再生心脏愈合有关。了解胎儿心肌再生的机制可能会导致应用于改变心肌梗死后成人的反应。
The adult response to myocardial infarction results in inflammation, scar formation, left ventricular dilatation, and loss of regional and global function. Regenerative scarless healing has been demonstrated in fetal dermis and tendon and is associated with diminished inflammation. We hypothesized that following fetal myocardial infarction there would be minimal inflammation, regenerative healing, and preservation of function. Anteroapical myocardial infarction encompassing 20% of the left ventricle were created in adult or early gestation fetal sheep. Myocardial function was serially assessed using quantitative echocardiography. Infarct architecture was examined histologically for evidence of scar formation. Cellular inflammation, cellular proliferation, and apoptosis were assessed using immunohistochemistry. In the adult sheep 4 weeks following myocardial infarction, there was a significant decline in ejection fraction (41±7.4% to 26±7.4%, p<0.05), and the akinetic myocardial segment increased in size (6.9±0.8 cm to 7.9±1.1 cm, p<0.05). In contrast, there was no decline in the fetal ejection fraction (53±8.1% to 55±8.8%) and no akinetic fetal myocardial segment 4 weeks post-infarction. The fetal infarcts lacked an inflammatory cell infiltrate and healed with minimal fibrosis, compared to the adults. Fetal infarcts also demonstrated BrdU+ proliferating cells, including cardiomyocytes, within the infarct. These data demonstrate that the fetal response to myocardial infarction is dramatically different than the adult and is characterized by minimal inflammation, lack of fibrosis, myocardial proliferation, and restoration of cardiac function. Diminished inflammation is associated with fetal regenerative cardiac healing following injury. Understanding the mechanisms involved in fetal myocardial regeneration may lead to applications to alter the adult response following myocardial infarction.
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影响因子：
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