A SNO storm in skeletal muscle

被引：29

作者：

Stamler, Jonathan S. ^{[1
,2
]}

Sun, Qi-An ^{[1
]}

Hess, Douglas T. ^{[1
]}

机构：

[1] Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA

[2] Duke Univ, Med Ctr, Dept Biochem, Durham, NC 27710 USA

来源：

CELL | 2008年 / 133卷 / 01期

关键词：

D O I：

10.1016/j.cell.2008.03.013

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：33 / 35

页数：3

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