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病毒基因转移的antiapoptotic因子Bcl-2可以防止慢性心脏衰竭
Subhasis Chatterjee1, Allan S Stewart, Lawrence T Bish
1Division of Cardiothoracic Surgery, University of Pennsylvania School of Medicine, Philadelphia, Pa 19104, USA.
Circulation
|October 2, 2002
概括
基因转移Bcl-2通过减少细胞亡和重塑,有效地保持心脏功能和结构缺血后,为后缺血性心力衰竭提供潜在的治疗方法.
科学领域:
- 心血管研究研究心血管研究
- 基因治疗 基因治疗
- 分子心脏病学分子心脏病学
背景情况:
- 亡有助于心力衰竭后的缺血和慢性重塑.
- 病毒基因转移Bcl-2的目的是阻止细胞亡并保持心脏功能.
研究的目的:
- 评估体内腺-Bcl-2基因转移在预防亡和在缺血后保持心室几何和功能的有效性.
- 评估Bcl-2基因转移对心脏重塑和心力衰竭进展的长期影响.
主要方法:
- 使用了区域性缺血-再输血的子模型.
- 实验组接受了adeno-Bcl-2;对照组接受了adeno-null.
- 通过心声学和声微仪评估心脏功能;在6周评估细胞亡和心室重塑.
主要成果:
- 接受Bcl-2治疗的子在缺血病后的2,4周和6周保持了更高的射出分数和上边界区域的分数缩短.
- 在Bcl-2组中观察到左心室 (LV) 几何结构的显著保存,扩张和壁薄化减少.
- 与对照组相比,Bcl-2组中发现了减少的亡和心室重塑,在3天内没有急性功能差异.
结论:
- 在体内Bcl-2基因转移在缺血后保留了LV功能和几何,这表明了对晚期后缺血性心力衰竭的潜在治疗策略.
- 在6周观察到的好处归因于Bcl-2-介导的亡减少和随后的心室重塑.
- 亚-Bcl-2的使用为缓解心力衰竭进展后缺血症提供了一个有希望的方法.
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