Analysis of ventricular hypertrabeculation and noncompaction using genetically engineered mouse models.
Analysis of ventricular hypertrabeculation and noncompaction using genetically engineered mouse models.
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DOI：
10.1007/s00246-009-9406-5
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发表时间：
2009-07
影响因子：
1.6
通讯作者：
Shou, Weinian
中科院分区：
文献类型：
--
作者：
Chen, Hanying;Zhang, Wenjun;Li, Deqiang;Cordes, Tim M.;Payne, R. Mark;Shou, Weinian
心室小梁形成和致密化是产生功能正常的心室壁的许多基本步骤中的两个。小梁形成的显著减少通常与心室致密带缺陷（发育不良的壁）有关，这通常导致胚胎心力衰竭和早期胚胎死亡。相比之下，过度小梁形成和缺乏心室壁致密化（致密化不全）是与左心室致密化不全（LVNC）相关的心脏胚胎发生中的密切相关缺陷，LVNC是一种遗传异质性疾病。在这里，我们总结了我们最近的研究结果，通过分析几个基因工程小鼠模型，有缺陷的心脏小梁形成和压实。我们的数据表明，细胞生长和分化信号通路是这些心室形态发生事件的关键。
Ventricular trabeculation and compaction are two of the many essential steps for generating a functionally competent ventricular wall. A significant reduction in trabeculation is usually associated with ventricular compact zone deficiencies (hypoplastic wall), which commonly leads to embryonic heart failure and early embryonic lethality. In contrast, hypertrabeculation and lack of ventricular wall compaction (noncompaction) are closely related defects in cardiac embryogenesis associated with left ventricular noncompaction (LVNC), a genetically heterogenous disorder. Here we summarize our recent findings through the analyses of several genetically engineered mouse models that have defects in cardiac trabeculation and compaction. Our data indicate that cellular growth and differentiation signaling pathways are keys in these ventricular morphogenetic events.
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