Haploinsufficiency of Hand1 improves mice survival after acute myocardial infarction through preventing cardiac rupture
Haploinsufficiency of Hand1 improves mice survival after acute myocardial infarction through preventing cardiac rupture
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Hand1的单倍体不足通过预防心脏破裂提高急性心肌梗塞后小鼠的存活率
DOI：
10.1016/j.bbrc.2016.09.012
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发表时间：
2016
影响因子：
3.1
通讯作者：
Dong Jianzeng
中科院分区：
文献类型：
--
作者：
Lu Shuangshuang;Du Pan;Shan Congjia;Wang Yaohe;Ma Changsheng;Dong Jianzeng
以前的研究表明，缺血性心肌病中的Hand 1水平明显低于正常心脏组织。Hand 1降低在心肌梗死中的作用尚不清楚。本研究旨在探讨Hand 1单倍不足对心肌梗死后小鼠心脏的影响。对（Hand 1 +/−）小鼠和野生型同窝小鼠（对照）进行假手术或结扎左前降支冠状动脉以诱导急性心肌梗死（AMI）。−术后第一周，小鼠左心室游离壁破裂的发生率低于对照组小鼠。然后，我们发现Hand 1 +/−小鼠的MMP 9活性和心肌细胞凋亡比对照小鼠低。这些都有助于AMI后Hand 1单倍功能不全的保护作用。
Previous studies have demonstrated a significantly lower level ofHand1in ischemic cardiomyopathy than in normal heart tissue. The role of decreased Hand1 in myocardial infarction remains unclear. This study was designed to investigate the effects of haploinsufficiency ofHand1on mouse heart after myocardial infarction.8-10 weeks old male heterozygousHand1-deficient (Hand1+/−) mice and wild-type littermates (control) were subjected to sham operation or ligation of the left anterior descending coronary artery to induce acute myocardial infarction (AMI).Hand1+/−mice have low incidence of left ventricular free wall rupture in the first week after operation than control mice. Then we found lower MMP9 activity and less cardiomyocytes apoptosis inHand1+/−than in control mice. All of these contribute to the protection role of haploinsufficiency ofHand1after AMI.