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 | Size | Format | Existing users please |
---|---|---|---|---|
Regulation.pdf | 1.03 MB | Adobe PDF | Request a copy |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.