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通过与线粒体相关的铁致死,VDAC2恶化参与了败血症诱导的心肌功能障碍

Han She^1,2, Lei Tan^1,2, Yuanlin Du²

¹State Key Laboratory of Trauma, Burns and Combined Injury, Shock and Transfusion Department, Daping Hospital, Army Medical University, Chongqing400042, China.

International journal of biological sciences

|July 7, 2023

概括

败血症引起的心肌功能障碍涉及VDAC2恶化升高,导致铁亡和心脏损伤. 以TPP-AAV等疗法针对这种修饰显示出治疗败血症相关心脏问题的前景.

科学领域:

生物化学生物化学
心脏病学心脏病学
分子生物学分子生物学

背景情况:

败血症引起的心肌功能障碍 (SIMD) 是一种严重的疾病,其机制不明确,治疗方法很少.
了解SIMD的分子基础对于开发有效疗法至关重要.

研究的目的:

为了研究电压依赖性离子通道2 (VDAC2) malonylation在SIMD中的作用.
探索向VDAC2恶结合的治疗潜力.

主要方法:

败血症模型是在体外和体内使用结和穿孔和脂聚糖化物 (LPS) 建立的.
使用质谱学和基于LC-MS的代谢学分析了VDAC2恶化,恶-CoA水平和铁化.
用分子动力学模拟和循环二元化来研究VDAC2的结构和功能.

主要成果:

在败血症模型中,VDAC2 lysine malonylation显著增加.
VDAC2恶化改变了它的N端结构,导致线粒体功能障碍,ROS增加和铁亡.
马洛尼尔-CoA被确定为VDAC2马洛尼化诱导剂;其抑制降低了铁亡并缓解了SIMD.
针对线粒体的纳米材料TPP-AAV抑制了VDAC2恶化和改善了心肌功能障碍.

结论:

VDAC2恶性化是败血症诱导的心肌功能障碍的一个关键因素.
针对VDAC2恶化,可能通过TPP-AAV等策略,为SIMD提供了一个有前途的治疗途径.

关键词:

铁化是铁化的一种.马洛尼尔-甲是一种马洛尼化是一种不良的.败血症这是一种败血症.在VDAC2中,它是VDAC2.

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