Nitric oxide and endoplasmic reticulum stress
- VernacularTitle:一氧化氮和内质网应激
- Author:
Jing CHEN
;
Jiong QIN
;
Ying HAN
;
Xiaoyan LIU
- Publication Type:Journal Article
- Keywords:
Apoptosis;
Calcium;
Endoplamic reticulum;
Nitric oxide
- From:
Chinese Journal of Pathophysiology
2000;0(11):-
- CountryChina
- Language:Chinese
-
Abstract:
Nitric oxide (NO) is a multifunctional biomolecule involved in a variety of physiological and pathological processes, including regulation of blood vessel dilatation and function as a neurotransmitter. However, a large amount of NO is toxic to the host and causes several diseases such as cardiovascular system diseases, septic shock, and diabetes mellitus. 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 disturbs 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 is involved in the pathogenesis of various diseases.
