The RGK (Rad, Rem, Rem2 and Gem/Kir) family of small GTPases are potent endogenous inhibitors of voltage-gated Ca²⁺ channels (VGCCs). While the impact of RGK proteins on cardiac physiology has been investigated extensively, much less is known regarding their influence on skeletal muscle biology. Thus, the purpose of this article is to establish a basis for future investigation into the role of RGK proteins in regulating the skeletal muscle excitation-contraction (EC) coupling complex via modulation of the L-type Ca_V1.1 VGCC. The pathological consequences of elevated muscle RGK protein expression in Type II Diabetes, Amyotrophic Lateral Sclerosis (ALS), Duchenne's Muscular Dystrophy and traumatic nerve injury are also discussed.

^{RGK（Rad、Rem、Rem2 和 Gem/Kir）家族的小 GTP 酶是电压门控 Ca 2+}通道 (VGCC)的有效内源性抑制剂。虽然已经广泛研究了 RGK 蛋白对心脏生理学的影响，但对其对骨骼肌生物学的影响知之甚少。因此，本文的目的是为未来研究 RGK 蛋白通过调节 L 型 Ca _V 1.1 VGCC 在调节骨骼肌兴奋-收缩 (EC) 耦合复合物中的作用奠定基础。还讨论了在 II 型糖尿病、肌萎缩侧索硬化症 (ALS)、杜氏肌营养不良症和外伤性神经损伤中肌肉 RGK 蛋白表达升高的病理后果。