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Mechanism od Cardiac Hypertrophy ; The Efficacy of Gene Therapy in Cardiac Hypertrophy

心脏肥大的机制；

基本信息

批准号：
08457350
负责人：
TAKAHASHI Toshiki
金额：
$ 4.03万
依托单位：
Osaka University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
1996
资助国家：
日本
起止时间：
1996 至 1997
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-08457350/
关键词：
Cardiac Hypertrophy Heart Failure Gene expression

项目摘要

Myocardial hypertrophy is a basic adaptive mechanism of the heart to compensate for an increased mechanical load. Heart failure is final presentation of cardiovascular disease, such as coronary artery disease, hypertension, valvular heart disease, myocarditis and others. The pathogenetic mechanisms responsible for the transition to cardiac dysfunction and heart failure are not well understood. Volume-overloaded rat hearts were established by A-V shunt between abdominal aorta and inferior caval vein. Immunohistochemical investigations of proto-oncogene proteins were performed in the presence. The myocytes of volume-overloaded hearts were significantly larger in diameter than control hearts on 14th day after A=V shunt. The weight of volume-overloaded hearts was also significantly larger than control hearts. In nuclei of myocytes of volume-overloaded hearts, the maximum expression of Fos and Myc protein was observed on the 2nd day after A-V shunt. After the 2nd day, the expression decreased gradually. In the human heart, however, it has not been clarified whether these proto-oncogenes are related to contractile impairment and structural alteration of the myocardium. The present study is designed to investigate the relationship between the C-Myc protein expression in the myocardium and the myocardial contractile dysfunction in patients with chronic aortic regurgitation. C-Myc was detected in nine of 12 present patients but in none of the normal controls. The degree of C-Myc expression had significant positive correlations with EF and ESS/ESVI and significant negative correlations with ESVI,CD and FC,which suggested that the degree of C-Myc expression may have a significant negative correlation with myocardial contractility and myocardial hypertrophy. Conclusion : C-Myc expression may be related to the pathogenesis of myocardial remodeling in patients with chronic aortic regurgitation.

心肌肥大是心脏补偿机械负荷增加的基本适应机制。心力衰竭是冠心病、高血压、心脏瓣膜病、心肌炎等心血管疾病的最终表现。导致向心功能不全和心力衰竭转变的发病机制尚不清楚。采用腹主动脉-下腔静脉动静脉分流术建立容量超负荷大鼠心脏模型。原癌基因蛋白的免疫组织化学研究进行了存在。A=V分流术后第14天，容量负荷组心肌细胞直径明显大于对照组。容量超负荷心脏的重量也明显大于对照心脏。在容量超负荷心肌细胞核中，Fos和Myc蛋白的表达在房室分流后第2天达到高峰。第2天以后，表达逐渐减少。然而，在人类心脏中，这些原癌基因是否与心肌的收缩障碍和结构改变有关尚不清楚。本研究旨在探讨慢性主动脉瓣关闭不全患者心肌C-Myc蛋白表达与心肌收缩功能障碍的关系。C-Myc在12例患者中的9例中检测到，但在正常对照组中没有检测到。C-Myc表达程度与EF、ESS/ESVI呈显著正相关，与ESVI、CD、FC呈显著负相关，提示C-Myc表达程度可能与心肌收缩力、心肌肥厚呈显著负相关。结论：C-Myc表达可能与慢性主动脉瓣关闭不全患者心肌重构的发生有关。