Content area

Abstract

Nitric oxide synthases (NOS) are crucial enzymes responsible for the production of nitric oxide (NO), a signaling molecule with essential roles in vascular regulation, immune defense, and neurotransmission. The three NOS isoforms, endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS (iNOS), are tightly regulated by inflammatory mediators and cellular signaling pathways. While physiological NO production is vital for maintaining homeostasis, dysregulated NOS activity contributes to the pathogenesis of numerous diseases, including cardiovascular disorders, neurodegenerative conditions, and cancer. Recent advances in understanding the molecular mechanisms of NOS regulation have unveiled novel therapeutic opportunities, including isoform-specific modulators, upstream pathways, and nanotechnology-enhanced delivery systems. This review highlights these advancements, offering insights into how targeting NOS and its regulatory network can enable precise and effective therapeutic strategies for managing inflammation-driven pathologies.

Details

1009240
Title
Advances in the Regulation of Inflammatory Mediators in Nitric Oxide Synthase: Implications for Disease Modulation and Therapeutic Approaches
Volume
26
Issue
3
First page
1204
Publication year
2025
Publication date
2025
Publisher
MDPI AG
Place of publication
Basel
Country of publication
Switzerland
ISSN
16616596
e-ISSN
14220067
Source type
Scholarly Journal
Language of publication
English
Document type
Journal Article
Publication history
 
 
Online publication date
2025-01-30
Milestone dates
2024-12-31 (Received); 2025-01-28 (Accepted)
Publication history
 
 
   First posting date
30 Jan 2025
ProQuest document ID
3165902750
Document URL
https://www.proquest.com/scholarly-journals/advances-regulation-inflammatory-mediators-nitric/docview/3165902750/se-2?accountid=208611
Copyright
© 2025 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
Last updated
2025-07-24
Database
ProQuest One Academic