Muscle KATP channels: recent insights to energy sensing and myoprotection.
Muscle KATP channels: recent insights to energy sensing and myoprotection.
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DOI：
10.1152/physrev.00027.2009
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发表时间：
2010-07
影响因子：
33.6
通讯作者：
Nichols CG
中科院分区：
文献类型：
--
作者：
Flagg TP;Enkvetchakul D;Koster JC;Nichols CG
ATP敏感性（KATP）通道存在于心肌、骨骼肌和平滑肌细胞的表面和内膜，在肌细胞代谢和电活动之间提供独特的反馈。在这样做时，它们可以在控制收缩性中发挥重要作用，特别是当细胞能量学受到损害时，保护组织免受钙超载和纤维损伤，但这种保护的代价可能是增强的血管活性。作为Kir6.1或Kir6.2孔形成亚基与调节磺酰脲受体亚基SUR1或SUR2的复合物产生，KATP通道在不同组织中的差异组装引起组织特异性生理和药理学调节，并因此引起收缩性的组织特异性药理学控制。在过去的十年里，人们对肌肉KATP通道的调节和作用有了深入的了解，这在很大程度上是由对小鼠的研究驱动的，在这些研究中，通道活性的蛋白质决定簇被删除或修饰。到目前为止，很少有人类疾病与肌肉KATP活性的改变有关，但转基因动物对不同肌肉类型中异常通道活性的可能病理作用提供了重要的见解。
ATP-sensitive (KATP) channels are present in the surface and internal membranes of cardiac, skeletal and smooth muscle cell, and provide a unique feedback between muscle cell metabolism and electrical activity. In so doing, they can play an important role in the control of contractility, particularly when cellular energetics are compromised, protecting the tissue against calcium overload and fiber damage, but the cost of this protection may be enhanced arrhythmic activity. Generated as complexes of Kir6.1 or Kir6.2 pore-forming subunits with regulatory sulfonylurea receptor subunits, SUR1 or SUR2, the differential assembly of KATP channels in different tissues gives rise to tissue-specific physiological and pharmacological regulation, and hence to the tissue-specific pharmacological control of contractility. The last ten years have provided insights to the regulation and role of muscle KATP channels, in large part driven by studies of mice in which the protein determinants of channel activity have been deleted or modified. As yet, few human diseases have been correlated with altered muscle KATP activity, but genetically modified animals give important insights to likely pathological roles of aberrant channel activity in different muscle types.
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