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Translating the oxidative stress hypothesis into the clinic: NOX versus NOS
Melanie E Armitage1, Kirstin Wingler, Harald H H W Schmidt
1Centre for Vascular Health, Department of Pharmacology, Monash University, Building 13E, Wellington Rd, Clayton, Victoria 3800, Australia.
Abstract:
Cardiovascular diseases remain the leading cause of death in industrialised nations. Since the pathomechanisms of most cardiovascular diseases are not understood, the majority of therapeutic approaches are symptom-orientated. Knowing the molecular mechanism of disease would enable more targeted therapies. One postulated underlying mechanism of cardiovascular diseases is oxidative stress, i.e. the increased occurrence of reactive oxygen species such as superoxide. Oxidative stress leads to a dysfunction of vascular endothelium-dependent protective mechanisms. There is growing evidence that this scenario also involves impaired nitric oxide (NO)-cyclic GMP signalling. Out of a number of enzyme families that can produce reactive oxygen species, NADPH oxidases stand out, as they are the only enzymes whose sole purpose is to produce reactive oxygen species. This review focuses on the clinically validated targets of oxidative stress, NO synthase (NOS) and the NO receptor, soluble guanylate cyclase as well as the source of ROS, e.g. NADPH oxidases. We place recent knowledge in the function and regulation of these enzyme families into clinical perspective. For a comprehensive overview of the biology and pharmacology of oxidative stress and possible other sources and targets, we refer to other literature overviews.
Insights
Oxidative stress, driven by reactive oxygen species (ROS), impairs nitric oxide (NO) signaling, contributing to cardiovascular diseases. Targeting NADPH oxidases, NO synthase, and soluble guanylate cyclase offers potential for novel therapies.
Area of Science:
- Cardiovascular medicine
- Molecular biology
- Biochemistry
Background:
- Cardiovascular diseases are a leading cause of death globally.
- Current treatments are often symptom-oriented due to poorly understood disease mechanisms.
- Oxidative stress, characterized by increased reactive oxygen species (ROS), is implicated in cardiovascular dysfunction.
Purpose of the Study:
- To review the role of oxidative stress in cardiovascular diseases.
- To examine the function and regulation of key enzymes involved in ROS production and signaling.
- To place recent knowledge into clinical perspective for potential therapeutic targets.
Main Methods:
- Literature review focusing on oxidative stress, nitric oxide (NO), and cyclic GMP pathways.
- Analysis of the role of NADPH oxidases as a primary source of ROS.
- Examination of NO synthase (NOS) and soluble guanylate cyclase (sGC) as clinically validated targets.
Main Results:
- Oxidative stress disrupts vascular endothelium-dependent protective mechanisms.
- Impaired nitric oxide (NO)-cyclic GMP signaling is a key feature of this scenario.
- NADPH oxidases are identified as the sole enzymes dedicated to ROS production.
Conclusions:
- Understanding the molecular mechanisms of cardiovascular diseases, particularly the role of oxidative stress, is crucial for developing targeted therapies.
- NADPH oxidases, NOS, and sGC represent clinically relevant targets for intervention.
- Further research into these pathways could lead to more effective treatments for cardiovascular diseases.
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