A SNO storm in skeletal muscle.
Dysregulated S-nitrosylation of proteins characterizes a broad array of human disorders, but its role in disease etiology is not well understood. Two new studies (Durham et al., 2008; Bellinger et al., 2008) now show that hyper-S-nitrosylation of the ryanodine receptor calcium release channel (RyR1) in skeletal muscle disrupts calcium ion flux. This disruption underlies the impaired contractility and cellular damage of skeletal muscle during strenuous exercise and in a spectrum of congenital muscle disorders including malignant hyperthermia.
Stamler
Jonathan S
JS
Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA. staml001@mc.duke.edu
Sun
Qi-An
QA
Hess
Douglas T
DT
D000818:Animals; D002118:Calcium / Q000378:metabolism; D018883:Heat Stroke / Q000378:metabolism; D006801:Humans; D008305:Malignant Hyperthermia / Q000378:metabolism; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000473:pathology*; D015538:Nitrosation; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism
D019837:Ryanodine Receptor Calcium Release Channel; D002118:Calcium