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AMPKγ的S-化会损害冠状动脉附带循环,并破坏VSMC重编程

Wenwu Bai¹, Tao Guo¹, Han Wang¹

¹National Key Laboratory for Innovation and Transformation of Luobing Theory; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China.

|January 4, 2024

概括

化应激通过S-化AMP激活蛋白激酶 (AMPK) 扰乱心脏附带循环,损害血管光滑肌细胞重编程和缺血后血流恢复.

科学领域:

心血管生物学心血管生物学
分子医学是分子医学.
血管生理学血管生理学

背景情况:

副侧循环对于缺血性心脏的恢复至关重要,它依赖于血管光滑肌细胞 (VSMC) 现型恢复.
AMP激活蛋白激酶 (AMPK) 调节VSMC表型,但其在化应激下附带循环中的作用尚不清楚.

研究的目的:

调查AMPK的S-化是否会损害附带循环.
阐明化应激影响VSMC重编程和附带血流的机制.

主要方法:

在小鼠和Apoe-/-小鼠接受缺血/心肌梗塞 (RI/MI) 的研究.
评估冠状动脉附带血流 (CCBF),VSMC表型和AMPK活动.
诱导性氧化合成酶 (iNOS) 和AMPK (C130A突变) 的基因操纵.

主要成果:

酸甘油降低了CCBF,损害了VSMC恢复,并增加了老鼠的心脏病发作的大小,与AMPK活性降低有关.
氧化 (NO) 在Cys131处S-化AMPK,降低AMP的敏感性.
防止AMPK的S-化或iNOS缺陷,防止VSMC重编程中断.
血糖过高/血糖过高增加了AMPK的S-化,降低了CCBF,并恶化了心脏损伤,因iNOS缺乏或AMPK突变表达而受到影响.

结论:

化应激通过AMPK S-化破坏冠状动脉附带循环.
这种机制与诸如高血糖和高血糖等疾病有关.
向AMPK S-化可能为缺血性心脏病提供治疗潜力.

关键词:

由AMP激活的蛋白激酶激活的蛋白激酶担保的流通担保的流通亚酸性压力是一种压力.现型复原现型复原现型复原血管光滑肌细胞血管光滑肌细胞

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