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

Mitochondrial targets for volatile anesthetics against cardiac ischemia-reperfusion injury.
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DOI:
10.3389/fphys.2014.00341
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发表时间:
2014
影响因子:
4
通讯作者:
Camara AK
Camara AK
中科院分区:
医学2区
文献类型:
--
作者:
Agarwal B;Stowe DF;Dash RK;Bosnjak ZJ;Camara AK

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线粒体是细胞功能的关键调节剂,并且越来越多地被认为是最终决定细胞生存和细胞死亡之间平衡的近端传感器和效应器。挥发性麻醉剂 (VA) 长期以来因其心脏保护作用而闻名,改善线粒体和细胞功能以及减少心脏缺血和再灌注 (IR) 损伤期间的坏死和凋亡细胞死亡就证明了这一点。 VA 赋予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显现,因此了解 VA 诱导的细胞保护机制是否在线粒体水平上介导非常重要。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) 复合物的直接影响是介导心脏保护的潜在目标。这篇综述对 VA 在线粒体通道/转运蛋白和 ETC 蛋白上传递的靶标进行了综合概述,这些靶标可以为阳离子调节和稳态、线粒体生物能学以及氧化还原信号传导中的活性氧 (ROS) 发射提供基础,从而在 IR 损伤期间保护心脏细胞。
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.
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