Journal
CELL
Volume 133, Issue 1, Pages 33-35Publisher
CELL PRESS
DOI: 10.1016/j.cell.2008.03.013
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Funding
- NHLBI NIH HHS [R01-HL059130] Funding Source: Medline
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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.
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