Rush University Medical Center, Department of Molecular Biophysics & Physiology, Section of Cellular Signaling, 1750 West Harrison Street, Chicago, IL 60612, USA.
J Mol Cell Cardiol. 2013 May;58:53-8. doi: 10.1016/j.yjmcc.2013.01.011. Epub 2013 Jan 28.
In cardiac muscle cells, ryanodine receptor (RyR) mediated Ca(2+) release from the sarcoplasmic reticulum (SR) drives the contractile apparatus. Spontaneous bouts of inter-RyR Ca(2+) induced Ca(2+) release (CICR) generate an elemental unit of SR Ca(2+) release called a spark. Sparks are localized events that terminate soon after they begin. The local control of sparks is not clearly understood. In this article, we review the potential regulatory role that the changing single RyR Ca(2+) current may play. Moreover, we aggregate RyR data into a working scheme of inter-RyR CICR current control of sparks and a potential inter-RyR CICR termination mechanism that we call pernicious attrition.
在心肌细胞中，兰尼碱受体（RyR）介导的肌浆网（SR）内钙离子释放驱动收缩装置。RyR 间自发的钙离子诱导钙离子释放（CICR）产生了一个被称为火花的 SR 钙离子释放的基本单位。火花是局部事件，在开始后很快就会结束。火花的局部控制尚不清楚。在本文中，我们回顾了不断变化的单个 RyR 钙离子流可能发挥的潜在调节作用。此外，我们将 RyR 数据汇总到一个工作方案中，即 RyR 间 CICR 电流控制火花，以及我们称之为恶性损耗的潜在 RyR 间 CICR 终止机制。
