Pathophysiological Role of S-Nitrosylation and Transnitrosylation Depending on S-Nitrosoglutathione Levels Regulated by S-Nitrosoglutathione Reductase.
10.4062/biomolther.2018.179
- Author:
Min Sik CHOI
1
Author Information
1. Lab of Pharmacology, College of Pharmacy, Dongduk Women's University, Seoul 02748, Republic of Korea. mschoi@dongduk.ac.kr
- Publication Type:Review
- Keywords:
Nitric Oxide;
S-nitrosylation;
Transnitrosylation;
GSNO;
GSNOR
- MeSH:
Cell Proliferation;
Drug Therapy;
Homeostasis;
Humans;
Inflammation;
Nitric Oxide;
Oxidoreductases*;
Pathologic Processes;
S-Nitrosoglutathione*
- From:Biomolecules & Therapeutics
2018;26(6):533-538
- CountryRepublic of Korea
- Language:English
-
Abstract:
Nitric oxide (NO) mediates various physiological and pathological processes, including cell proliferation, differentiation, and inflammation. Protein S-nitrosylation (SNO), a NO-mediated reversible protein modification, leads to changes in the activity and function of target proteins. Recent findings on protein-protein transnitrosylation reactions (transfer of an NO group from one protein to another) have unveiled the mechanism of NO modulation of specific signaling pathways. The intracellular level of S-nitrosoglutathione (GSNO), a major reactive NO species, is controlled by GSNO reductase (GSNOR), a major regulator of NO/SNO signaling. Increasing number of GSNOR-related studies have shown the important role that denitrosylation plays in cellular NO/SNO homeostasis and human pathophysiology. This review introduces recent evidence of GSNO-mediated NO/SNO signaling depending on GSNOR expression or activity. In addition, the applicability of GSNOR as a target for drug therapy will be discussed in this review.
