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内源补充1q结合蛋白 (C1qbp) 调节线粒体透性过渡和心肌梗塞后的重塑和功能障碍

Manuel Gutiérrez-Aguilar¹, Paula J Klutho², Rodrigo Aguayo-Ortiz³

¹Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO 65211, USA; Departamento de Bioquímica, Facultad de Química, Universidad Nacional Autónoma de México, Mexico City 04510, Mexico.

Journal of molecular and cellular cardiology

|August 29, 2024

概括

补充1q结合蛋白 (C1qbp) 调节线粒体透性过渡 (MPT) 孔口的开放. 失去了C1qbp使心脏敏感于肌心梗塞后的损伤和功能障碍,独立于MPT.

科学领域:

心血管生物学心血管生物学
线粒体医学线粒体医学
细胞死亡途径细胞死亡途径

背景情况:

线粒体透性转换 (MPT) 孔在心脏损伤后调节细胞死亡方面至关重要.
环素D (CypD) 是已知的MPT孔隙开放的促进剂.
补充1q结合蛋白 (C1qbp) 之前被确定为一种与CypD相互作用的分子,可以在体外抑制MPT依赖的细胞死亡.

研究的目的:

在体内调查C1qbp在调节MPT孔隙和心肌细胞死亡中的作用.
为了确定C1qbp是否影响MPT孔隙对和心脏功能的敏感性,在心肌梗塞后.

主要方法:

生成特定于心脏的C1qbp功能增益和丧失的小鼠模型.
评估线粒体功能,MPT孔隙对的敏感性和心脏形态.
在实验诱导的心肌梗塞后评估心脏病发作大小和心脏重塑.

主要成果:

过度表达C1qbp没有影响MPT,但减少了线粒体呼吸和ATP产生.
在C1qbp异构的小鼠 (C1qbp+/-) 中,MPT孔隙对的敏感性增加,基线线粒体功能没有变化.
与对照组相比,C1qbp+/-小鼠在心肌梗塞后表现出恶化的心脏功能障碍和痕形成.

结论:

C1qbp在MPT孔隙和线粒体功能的正常调节中发挥作用.
C1qbp在心肌梗塞后影响心脏重塑和功能障碍,可能是通过独立于其对MPT孔的直接影响的机制.

关键词:

线粒体中的线粒体.心肌梗塞的心脏病发作氧化酸化是一种氧化酸化.透性过渡的过渡过程

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