Figure 1.
A schematic illustration of the role of Ca
2+
in the development of skeletal muscle dysfunction in DMD. The two proposed pathways of Ca2+-induced muscle dysfunction include (A) increased SR Ca2+ leak and extracellular Ca2+ entry via (B) sarcolemmal membrane damage or (C) SOCE. Dihydropyridine receptor (DHPR), ryanodine receptor 1 (RyR1), sarcoplasmic reticulum Ca2+ ATPase (SERCA), mitochondrial reactive oxygen species (ROS), Orai Ca2+ release-activated Ca2+ modulator 1 (Orai1), stromal interaction molecule 1 (STIM1). Figure created with Biorender.com.