在成年小鼠中诱导心脏再生
Yuji Nakada1, Diana C Canseco1, SuWannee Thet1
1Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.
Nature
|November 8, 2016
概括
低氧可以通过减少DNA损伤和促进心肌细胞的增殖来刺激成年小鼠的心脏再生. 这一发现为心脏修复和再生医学提供了潜在的治疗策略.
科学领域:
- 心血管生物学
- 复原医学
- 分子心脏病学
背景情况:
- 成年哺乳动物的心脏在受伤后的再生能力有限,
- 最近的发现表明,成年人的心脏保留了一些自我更新的潜力,主要是通过心肌细胞的增殖.
- 心肌细胞的更新与有氧呼吸调节的氧化DNA损伤有关.
研究的目的:
- 通过全身性低氧化症抑制有氧呼吸是否可以诱导成年哺乳动物的心肌细胞增殖.
- 探索低氧症作为心脏再生治疗策略的潜力.
主要方法:
- 将小鼠逐渐暴露在严重的全身低氧症中 (氧气含量为7% 2周).
- 氧化代谢,反应性氧物种的产生和DNA损伤的评估.
- 在心肌梗塞后分析心肌细胞转移和心肌再生.
- 基因命运映射可以追踪新心肌细胞的起源.
主要成果:
- 低氧症抑制了氧化代谢,减少了活性氧物种和DNA损伤.
- 在成年小鼠中观察到心肌细胞转移的重新激活.
- 心肌梗塞后的低氧治疗促进了心脏再生,减少了纤维化,改善了心脏功能.
- 证实新形成的心肌源自现有的心肌细胞.
结论:
- 逐渐发生的全身性低氧症可以重新激活成年哺乳动物心脏的内生再生能力.
- 缺氧在再生医学中是一个有前途的治疗途径,
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