Jovanović Aleksandar, Jovanović Sofija
Division of Medical Sciences, Ninewells Hospital & Medical School, University of Dundee, Dundee DD1 9SY, UK.
Curr Opin Pharmacol. 2009 Apr;9(2):189-93. doi: 10.1016/j.coph.2008.11.003. Epub 2008 Dec 10.
SUR2A is an ATP-binding protein known to serve as a regulatory subunit of metabolic-sensing, cardioprotective sarcolemmal ATP-sensitive K(+) (K(ATP)) channels. It has been recently found that a moderate increase in expression of SUR2A protects the heart against different types of metabolic stresses, including ischaemia/reperfusion and hypoxia. Although the sarcolemmal K(ATP) channel is a multiprotein complex composed of many proteins in vivo, it seems that an increase in SUR2A levels is sufficient to increase the number of sarcolemmal K(ATP) channels. This effect of SUR2A could be due to SUR2A being the rate-limiting factor in generating fully composed sarcolemmal K(ATP) channels. An increased number of sarcolemmal K(ATP) channels seems to protect the heart by regulating action membrane potential, inhibiting Ca(2+) influx and preventing Ca(2+) overload, although an additional yet to be recognised mechanism independent of K(ATP) channels activity cannot be excluded.
SUR2A是一种ATP结合蛋白，已知它作为代谢感知、心脏保护的肌膜ATP敏感性钾离子（K(ATP)）通道的调节亚基。最近发现，SUR2A表达适度增加可保护心脏免受不同类型的代谢应激，包括缺血/再灌注和缺氧。尽管肌膜K(ATP)通道在体内是由多种蛋白质组成的多蛋白复合物，但似乎SUR2A水平的增加足以增加肌膜K(ATP)通道的数量。SUR2A的这种作用可能是由于SUR2A是生成完全组装的肌膜K(ATP)通道的限速因子。肌膜K(ATP)通道数量增加似乎通过调节动作膜电位、抑制Ca(2+)内流和防止Ca(2+)过载来保护心脏，尽管不能排除存在独立于K(ATP)通道活性的其他尚未被认识的机制。
