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钙超载作为心肌缺血再灌注损伤的重要机制之一，其形成原因与治疗策略一直是研究的热点。心肌遭受缺血再灌注后，参与细胞内钙循环的L-型电压依赖钙通道(L-type voltage-dependent calcium channel, L-VDCC)、肌浆网钙ATP酶2a (sarco/endoplasmic reticulum ATPase 2a, SERCA2a)和受磷蛋白(phospholamban, PLB)、Ryanodine受体2 (Ry R2)、Na+/Ca2+交换体、Na+/H+交换体等多种蛋白功能异常，导致舒张期[Ca2+]i上升，钙瞬变幅度降低，细胞出现钙超载。[Ca2+]i升高的过程大致可分为两个阶段：早期的[Ca2+]i升高过程(部分由钙通道介导)和晚期的[Ca2+]i升高过程(主要由Na+/Ca2+交换体介导)。L-VDCC活性增加参与钙超载的形成，但是L-VDCC蛋白在缺血再灌注过程中的分子变化机制尚不清楚。L-VDCC通道调控方式包括两类：自身调节和外源性调节，其中外源性调节蛋白PKG和PKA的调控不能解释细胞水平的L-VDCC活性增加现象，而在缺血再灌注过程中，钙依赖的失活(calcium-dependent inactivation, CDI)效应减弱、钙依赖的易化(calcium-dependent facilitation, CDF)效应增强、羧基远端部分肽链(distal carboxy terminus, DCT)的抑制效应减弱，这三种自身调节机制的改变引起L-VDCC活性的增加。因此，可以认为L-VDCC通道自身调控异常参与缺血再灌注损伤中心肌细胞钙超载的形成。
Calcium overload as one of the important mechanisms of myocardial ischemia-reperfusion injury, its formation and treatment strategies have been the hot spots. After myocardial ischemia and reperfusion, L-type voltage-dependent calcium channel (L-VDCC), sarco / endoplasmic reticulum ATPase 2a , SERCA2a) and phospholamban (PLB), Ryanodine receptor 2 (Ry R2), Na + / Ca2 + exchanger, Na + / H + exchanger and other proteins, leading to increased diastolic [Ca2 +] i, Transient amplitude decreased, the cells appear calcium overload. The process of [Ca2 +] i increase can be roughly divided into two stages: the early [Ca2 +] i up-regulation (partly mediated by calcium channels) and the late [Ca2 +] i up-regulation mainly due to Na + / Ca2 + exchange Body mediated). The increase of L-VDCC activity is involved in the formation of calcium overload, but the molecular mechanism of L-VDCC protein during ischemia-reperfusion is still unclear. There are two types of regulation of L-VDCC channels: autoregulation and extrinsic regulation. The regulation of exogenous regulatory proteins PKG and PKA can not explain the increase of L-VDCC activity at the cellular level. During the process of ischemia-reperfusion, The effect of calcium-dependent inactivation (CDI) was weakened, the effect of calcium-dependent facilitation (CDF) was enhanced, and the inhibitory effect of carboxyl distal carboxy terminus (DCT) Changes in these three self-regulatory mechanisms cause an increase in L-VDCC activity. Therefore, it can be considered that the abnormal regulation of L-VDCC channel participates in the formation of calcium overload in myocardial cells during ischemia-reperfusion injury.