CD38 缺乏通过协调抑制热和亡来缓解糖尿病心肌病症
Ling-Fang Wang1, Qian Li1, Ke Wen1
1National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Nanchang University, Nanchang 330031, China.
International journal of molecular sciences
|November 14, 2023
概括
缺少CD38通过减少通过NAD+/Sirt3/FOXO3a通路的细胞死亡来预防糖尿病心肌病. 这一发现为糖尿病中心脏并发症的管理提供了潜在的治疗点.
科学领域:
- 心血管生物学 心血管生物学
- 代谢疾病 代谢疾病
- 分子医学是分子医学.
背景情况:
- 糖尿病心肌病是一种糖尿病并发症,导致心力衰竭.
- CD38是一种NAD+酸酶,与心血管疾病有关,但其在糖尿病心肌病中的作用尚不清楚.
研究的目的:
- 研究CD38在糖尿病心肌病的发展中的作用.
- 探索CD38缺乏症在减轻糖尿病引起的心脏损伤方面的治疗潜力.
主要方法:
- 使用CD38淘汰赛 (CD38-KO) 的小鼠接受了高脂肪饮食和链毒素 (STZ) 注射.
- 评估心脏功能,心肌细胞亡,烧亡以及分子信号通路 (NAD+/Sirt3/FOXO3a).
主要成果:
- 缺少CD38显著保护糖尿病心肌病,改善心脏功能 (射出分数,分数缩短).
- CD38缺乏减少了心肌细胞亡和糖尿病或高葡萄糖/棕酸诱导的热亡.
- 在糖尿病小鼠心脏中观察到上调的CD38和下调的Sirt3; CD38缺乏增加了Sirt3和FOXO3a的表达.
结论:
- 缺乏CD38可以通过抑制亡和热亡来改善糖尿病心肌病.
- 保护作用通过NAD+/Sirt3/FOXO3a信号通路的激活来实现.
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