患有高血压BPH/2J的小鼠表现出性别特异的心力衰竭进展和晚年微血管稀缺症
Laena Pernomian1,2, Emily W Waigi1,2, Juliana M Parente1,2
1Department of Cell Biology and Anatomy, School of Medicine, Cardiovascular Translational Research Center, University of South Carolina, Columbia, South Carolina, United States.
概括
高血压在雄性和雌性小鼠中导致心力衰竭 (HF) 的原因不同. 男人发展HF减少喷射分数和稀缺,而女性发展HF保存喷射分数,显示不同的细胞动态.
科学领域:
- 心血管生物学心血管生物学
- 高血压研究研究 高血压研究
- 疾病中的性别差异.
背景情况:
- 心力衰竭 (HF) 是一个日益增长的健康负担,联系高血压和HFpEF的机制尚不清楚.
- 轻微减少喷射分数 (HFmrEF) 的HF中的性别差异因内皮细胞 (EC) 微血管稀缺而加剧.
- 保持喷射分数 (HFpEF) 的高血压在女性中更为普遍,高血压是主要的危险因素.
研究的目的:
- 用BPH/2J小鼠模型研究高血压引起的心力衰竭的性别特异机制.
- 为了测试这种假设,高血压的雄性小鼠发展HFmrEF与EC稀缺,而雌性发展HFpEF.
主要方法:
- 在雄性和雌性BPN/3J (对照) 和BPH/2J (高血压) 小鼠中评估血压,心脏功能 (心声图),心脏EC密度和SCa1+细胞.
- 使用免疫光学和心声回声学进行心脏评估.
主要成果:
- 在高血压发作之前,BPH/2J小鼠表现出心脏功能障碍.
- 在1.5年后,高血压BPH/2J小鼠表现出性别依赖的HF特征:雄性表现出HFmrEF特征和心脏EC稀缺,而雌性表现出HFpEF特征.
- 与高血压男性相比,雌性BPH/2J小鼠在冠状动脉中保留了SCa1+细胞.
结论:
- BPH/2J小鼠为高血压诱导的高血压特征提供了一个新的性别特异模型.
- 在这个模型中,性别之间观察到不同的内皮细胞和原始细胞动态.
- SCa1+细胞可能会影响左心室喷射率 (LVEF) 恶化,这表明心脏修复的潜在治疗点.
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