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线粒体靶点作为挥发性麻醉剂对抗心肌缺血再灌注损伤的作用。

Mitochondrial targets for volatile anesthetics against cardiac ischemia-reperfusion injury.

机构信息

Department of Anesthesiology, Medical College of Wisconsin Milwaukee, WI, USA.

Department of Anesthesiology, Medical College of Wisconsin Milwaukee, WI, USA ; Department of Physiology, Medical College of Wisconsin Milwaukee, WI, USA ; Cardiovascular Research Center, Medical College of Wisconsin Milwaukee, WI, USA ; Zablocki VA Medical Center Milwaukee, WI, USA ; Department of Biomedical Engineering, Marquette University Milwaukee, WI, USA.

出版信息

Front Physiol. 2014 Sep 16;5:341. doi: 10.3389/fphys.2014.00341. eCollection 2014.

DOI:10.3389/fphys.2014.00341
PMID:25278902
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4165278/
Abstract

Mitochondria are critical modulators of cell function and are increasingly recognized as proximal sensors and effectors that ultimately determine the balance between cell survival and cell death. Volatile anesthetics (VA) are long known for their cardioprotective effects, as demonstrated by improved mitochondrial and cellular functions, and by reduced necrotic and apoptotic cell death during cardiac ischemia and reperfusion (IR) injury. The molecular mechanisms by which VA impart cardioprotection are still poorly understood. Because of the emerging role of mitochondria as therapeutic targets in diseases, including ischemic heart disease, it is important to know if VA-induced cytoprotective mechanisms are mediated at the mitochondrial level. In recent years, considerable evidence points to direct effects of VA on mitochondrial channel/transporter protein functions and electron transport chain (ETC) complexes as potential targets in mediating cardioprotection. This review furnishes an integrated overview of targets that VA impart on mitochondrial channels/transporters and ETC proteins that could provide a basis for cation regulation and homeostasis, mitochondrial bioenergetics, and reactive oxygen species (ROS) emission in redox signaling for cardiac cell protection during IR injury.

摘要

线粒体是细胞功能的关键调节因子,越来越多的研究表明其作为近端传感器和效应器,最终决定细胞存活和死亡之间的平衡。挥发性麻醉剂(VA)以其心脏保护作用而闻名,其机制为改善线粒体和细胞功能,并减少心脏缺血再灌注(IR)损伤期间的坏死和凋亡细胞死亡。VA 发挥心脏保护作用的分子机制仍知之甚少。由于线粒体作为包括缺血性心脏病在内的疾病的治疗靶点的作用日益凸显,因此了解 VA 诱导的细胞保护机制是否在线粒体水平上发挥作用非常重要。近年来,大量证据表明 VA 对线粒体通道/转运蛋白功能和电子传递链(ETC)复合物的直接作用可能是介导心脏保护的潜在靶点。本文综述了 VA 对线粒体通道/转运蛋白和 ETC 蛋白的作用靶点,为阳离子调节和动态平衡、线粒体生物能学以及还原信号中活性氧(ROS)的产生提供了基础,从而为 IR 损伤期间心脏细胞的保护提供了依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b774/4165278/6c1aeeec5bba/fphys-05-00341-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b774/4165278/cf1c1301b6a1/fphys-05-00341-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b774/4165278/c82aa59b4a6c/fphys-05-00341-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b774/4165278/3d1eaa0d6d1c/fphys-05-00341-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b774/4165278/6c1aeeec5bba/fphys-05-00341-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b774/4165278/cf1c1301b6a1/fphys-05-00341-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b774/4165278/c82aa59b4a6c/fphys-05-00341-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b774/4165278/3d1eaa0d6d1c/fphys-05-00341-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b774/4165278/6c1aeeec5bba/fphys-05-00341-g0004.jpg

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