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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:1439.)
© 2006 American Heart Association, Inc.

Brief Reviews

Nitric Oxide and Endoplasmic Reticulum Stress

Tomomi Gotoh; Masataka Mori

From the Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Japan.

Correspondence to Dr Tomomi Gotoh, Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Honjo 1-1-1, Kumamoto 860-8556, Japan. E-mail tomomi{at}gpo.kumamoto-u.ac.jp

Series Editor: Joseph Loscalzo
Nitric Oxide Redux
ATVB In Focus

Previous Brief Reviews in this Series:

•Kim-Shapiro DB, Schlechter AN, Gladwin MT. Unraveling the reactions of nitric oxide, nitrite, and hemoglobin in physiology and therapeutics. 2006;26:697–705.
•Handy DE, Loscalzo J. Nitric oxide and posttranslational modification of the vascular proteome: S-nitrosation of reaction thiols. 2006;26:1207–1214.

Nitric oxide (NO) is a multifunctional biomolecule involved in a variety of physiological and pathological processes, including regulation of blood vessel dilatation and anti-arteriosclerotic effects. However, a large amount of NO is toxic to the host and causes several diseases such as apoptosis, septic shock, and diabetes mellitus. Inducible-form NO synthase is induced in inflammatory diseases, including insulitis and arteriosclerosis. Endoplasmic reticulum (ER) stress pathway was first identified as a cellular response pathway induced by the accumulation of unfolded proteins in ER to preserve ER functions. Later it was found that ER stress pathway is also activated by various cellular stresses to protect cells, but when stresses are severe, apoptosis is induced to remove damaged cells. It is reported that NO and reactive oxygen species disturb ER functions, then ER stress-mediated apoptosis pathway is activated. CHOP/GADD153, which belongs to C/EBP transcription factor family, is induced in this process and mediates apoptosis. ER stress pathway induced by NO can be involved in the pathogenesis of various vascular diseases.

Excess NO causes apoptosis through the ER stress pathway in some types of cells. It was found that the ER stress pathway is activated by various stresses, and when stresses are severe, apoptosis is induced. The NO-induced ER stress pathway may be involved in pathogenesis of various vascular diseases.

Key Words: apoptosis • Ca²⁺ • endoplasmic reticulum stress • nitric oxide

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