The Dystrophin-Glycoprotein Complex in the Prevention of Muscle Damage

Figure 1

Sources of calcium entry in dystrophic muscle. (1) Disruptions to the DGC can result in instability of the sarcolemma that permits calcium entry through membrane tears when the sarcolemma is stretched during lengthening muscle contractions. (2) Activity of calcium leak, stretch-activated, and various TRP channels has been shown to be increased in dystrophin-deficient muscle and their inhibition in vivo can improve dystrophic pathology. (3) The ryanodine receptor has recently been shown to be hypernitrosylated in mdx muscle which may result in an increased leak of calcium from the sarcoplasmic reticulum.