Please use this identifier to cite or link to this item: https://biore.bio.bg.ac.rs/handle/123456789/195
Title: Regulation of inducible Nitric Oxide synthase (iNOS) and its potential role in insulin resistance, diabetes and heart failure
Authors: Soskić, Sanja
Dobutović, Branislava
Sudar, Emina
Obradović, Milan
Nikolić, Dragana
Đorđević, Jelena 
Radak, Đorđe
Mikhailidis, Dimitri
Isenović, Esma
Keywords: Diabetes;Heart failure;Inducible nitric oxide synthase;Insulin resistance
Issue Date: 11-Oct-2011
Journal: Open Cardiovascular Medicine Journal
Abstract: 
Nitric oxide synthases (NOS) are the enzymes responsible for nitric oxide (NO) generation. NO is a reactive oxygen species as well as a reactive nitrogen species. It is a free radical which mediates several biological effects. It is clear that the generation and actions of NO under physiological and pathophysiological conditions are regulated and extend to almost every cell type and function within the circulation. In mammals 3 distinct isoforms of NOS have been identified: neuronal NOS (nNOS), inducible NOS (iNOS) and endothelial NOS (eNOS). The important isoform in the regulation of insulin resistance (IR) is iNOS. Understanding the molecular mechanisms regulating the iNOS pathway in normal and hyperglycemic conditions would help to explain some of vascular abnormalities observed in type 2 diabetes mellitus (T2DM). Previous studies have reported increased myocardial iNOS activity and expression in heart failure (HF). This review considers the recent animal studies which focus on the understanding of regulation of iNOS activity/ expression and the role of iNOS agonists as potential therapeutic agents in treatment of IR, T2DM and HF.
URI: https://biore.bio.bg.ac.rs/handle/123456789/195
DOI: 10.2174/1874192401105010153
Appears in Collections:Journal Article

Files in This Item:
File Description SizeFormat Existing users please
Regulation.pdf1.03 MBAdobe PDF
    Request a copy
Show full item record

SCOPUSTM   
Citations

140
checked on Oct 31, 2024

Google ScholarTM

Check

Altmetric

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.