Báo cáo khoa học: Nitric oxide in blood The nitrosative–oxidative disequilibrium hypothesis on the pathogenesis of cardiovascular disease

Authors:

Maqsood M. Elahi, Khalid M. Naseem, Bashir M. Matata

Field:

Cardiology, Biochemistry

Document Content:

This review article delves into the complex interplay between nitric oxide (NO), reactive oxygen species (ROS), and reactive nitrogen species (RNS) in the context of cardiovascular disease (CVD). It explores the hypothesis that an imbalance, or disequilibrium, between nitrosative and oxidative processes in the blood and cardiovascular system contributes significantly to the development and progression of CVD. The article discusses the molecular mechanisms, signaling pathways, and physiological implications of NO and its interactions with ROS/RNS, highlighting their roles in cellular function, inflammation, and tissue injury. It examines how altered NO bioavailability and signaling can lead to cardiovascular dysfunction, emphasizing the potential for therapeutic strategies targeting this NO/redox imbalance.

Detailed Table of Contents:

• Keywords
• Correspondence
• Abstract
• Introduction
• Nitric oxide and its interaction with oxygen
• Cellular/subcellular malfunction in signal transduction
• ROS/RNS axis
• Molecular basis of interaction
• Mitochondrial electron transport chain as a source of ROS?
• Signaling via cysteine thiols
• Transduction of NO-dependent activity via red blood cells
• Redox-sensitive transcriptional signaling pathways
• NO modulation of transcription factor activity
• Redox regulation of AP-1
• Redox regulation of NF-κB
• Peroxisome proliferator-activated receptors
• Cardiovascular sources of O2/ROS and NO/RNS
• NO/redox imbalance in CVD
• Cardiac NO signaling and NO-ROS competition in blood
• Conclusions
• References