在内热过程中对心脏再生能力的荷尔蒙控制的证据
Kentaro Hirose1,2, Alexander Y Payumo1,2, Stephen Cutie1,2
1Cardiovascular Research Institute and Department of Physiology, University of California, San Francisco, San Francisco, CA 94158, USA.
概括
由于甲状腺激素的增加, 哺乳动物的心脏再生失去了, 这项研究将甲状腺激素信号与心肌细胞循环停止和成年哺乳动物的再生能力降低联系在一起.
科学领域:
- 比较生物学
- 生理学
- 发育生物学
背景情况:
- 组织的再生潜力在物种和发育阶段之间有很大差异,机制不太清楚.
- 哺乳动物心脏再生在成年人中明显缺失,与心肌细胞循环停止和多重化相关.
- 哺乳动物内热的演变与这种再生能力的丧失相吻合.
研究的目的:
- 研究成年哺乳动物心脏再生潜力的损失的潜在机制.
- 探索新陈代谢,体温,甲状腺激素和心肌细胞增殖之间的关系.
- 确定甲状腺激素信号在心脏再生中的作用.
主要方法:
- 分析了41个物种的双胞胎心肌细胞数量,与新陈代谢率,体温和血清甲状腺素水平相关联.
- 研究了对成年小鼠甲状腺激素信号失活对心肌细胞多倍化和细胞周期退出的影响.
- 研究了外源性甲状腺激素对斑马鱼心脏再生的影响,这是一种以其再生能力而闻名的物种.
主要成果:
- 双胞胎心肌细胞的丰富性遵循克莱伯定律 (3/4级定律缩放) 并与代谢率,体温和甲状腺素水平相反相关.
- 在成年小鼠中,甲状腺激素信号的减少减少了心肌细胞的多重化,延迟了细胞周期的退出,并保持了心脏再生潜力.
- 给予斑马鱼的甲状腺激素抑制了它们的心脏再生的能力.
结论:
- 成年哺乳动物的心脏再生能力的丧失似乎是由甲状腺激素水平升高引发的.
- 在哺乳动物中获得内热可能涉及到通过甲状腺激素调解的心脏再生能力的权衡.
- 甲状腺激素信号是心肌细胞循环进展和心脏再生的关键调节者.
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