阿拉曼丁通过抑制铁灭症来抑制血管化
Zhanpeng Wen1, Jingbin Guo2, Keyang Li2
1Department of Cardiology, Laboratory of Heart Center, Heart Center, Zhujiang Hospital, Southern Medical University, Guangzhou, 510280, China; Guangdong Provincial Key Laboratory of Cardiac Function and Microcirculation, Guangdong Provincial Biomedical Engineering Technology Research Center for Cardiovascular Disease, Guangzhou, 510280, China; Department of Cardiology, Zhongshan People's Hospital, Zhongshan, 528403, China.
阿拉曼丁 (ALA) /mas关联的G蛋白结合受体D (MrgD) 通过向铁死来抑制血管化. 这一发现为治疗血管化提供了一个新的治疗策略,这是慢性病和糖尿病的常见并发症.
科学领域:
- 心血管生物学 心血管生物学
- 腎臟醫學 腎臟醫學
- 代谢疾病 代谢疾病
背景情况:
- 血管化是慢性病 (CKD),糖尿病和动脉样硬化的标志,显著增加心脏事件风险.
- 非正规的氨酸- ангиотензин系统 (RAS) 轴,阿拉曼丁 (ALA) /mas关联的G蛋白合受体D (MrgD),显示出心血管方面的益处,但其在血管化中的作用尚不清楚.
研究的目的:
- 研究ALA/MrgD对血管化的保护作用.
- 阐明潜在的机制,特别是铁灭的作用.
主要方法:
- 血管光滑肌细胞 (VSMC) 化是由高酸盐和引起的.
- 在小鼠中使用维生素D3诱导的大动脉化.
- 阿利沙林红色染色,含量测定和西部斑点分析以评估化和蛋白质表达.
- 研究了铁灭菌标志物 (ROS,MDA,SLC7A11,GPX4) 和铁灭菌抑制剂RSL3.3的作用.
主要成果:
- 在患有胸部化的患者中观察到较低的ALA血清水平.
- 在体外和体内,ALA治疗抑制了VSMC和动脉环化.
- 通过阻断MrgD,ALA的保护作用被废除了.
- VSMC化与铁亡有关,通过增加细胞死亡,ROS,MDA和减少SLC7A11/GPX4.4来证明这一点.
- ALA 抑制了铁和对抗了铁诱导的化.
结论:
- ALA/MrgD有效地抑制了血管光滑肌肉细胞和大动脉化.
- ALA/MrgD通过调节铁亡来发挥其保护作用.
- ALA/MrgD 途径为血管化提供了一个新的治疗标.
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