Abstract

Redox control is lost when the antioxidant defense system cannot remove abnormally high concentrations of signaling molecules, such as reactive oxygen species (ROS). Chronically elevated levels of ROS cause oxidative stress that may eventually lead to cancer and cardiovascular and neurodegenerative diseases. In this review, we focus on redox effects in the vascular system. We pay close attention to the subcompartments of the vascular system (endothelium, smooth muscle cell layer) and give an overview of how redox changes influence those different compartments. We also review the core aspects of redox biology, cardiovascular physiology, and pathophysiology. Moreover, the topic‐specific knowledgebase DES‐RedoxVasc was used to develop two case studies, one focused on endothelial cells and the other on the vascular smooth muscle cells, as a starting point to possibly extend our knowledge of redox control in vascular biology.

Highlights

  • Reactive oxygen species (ROS) and reactive nitrogen species (RNS) stimulate redox homeostasis mechanisms, and they are considered critical signaling molecules for maintaining cellular homeostasis

  • Endothelial reactive oxygen species (ROS) production has a prominent role in regulating the vascular redox homeostatic mechanisms in the vascular system

  • By understanding the ROS/RNS removal processes, we may influence the overall perturbing homeostatic functioning of the vascular endothelial system and the underlining consequence of a disbalance portraying as oxidative stress (OxS) in which it elevates inflammation and vascular remolding, activating the events for cardiovascular disease (CVD)

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Summary

Introduction

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) stimulate redox homeostasis mechanisms, and they are considered critical signaling molecules for maintaining cellular homeostasis.

Results
Conclusion
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