Oxidative Stress and Endothelial Function in Cardiovascular Health
Summary
The vascular endothelium forms the inner cellular lining of the circulatory system and orchestrates critical functions including regulation of vascular tone, barrier permeability and haemostatic balance. Endothelial cells maintain vascular homeostasis largely through production of nitric oxide (NO) and other endothelium-derived relaxing factors. Oxidative stress arises when reactive oxygen species (ROS) generated by mitochondria, NADPH oxidases and uncoupled nitric oxide synthases exceed antioxidant defences. Excessive ROS scavenge NO, yielding peroxynitrite and impairing vasodilatation. Concurrently, oxidative signals activate pro-inflammatory transcription factors such as NF-κB, upregulating adhesion molecules and chemokines that facilitate leukocyte recruitment. Over time, these events compromise barrier integrity, promote endothelial apoptosis and foster a pro-thrombotic, proliferative milieu, contributing to atherosclerosis, hypertension and microvascular complications in diabetes. Advances in non-invasive functional testing now enable early detection of endothelial impairment, offering prognostic insight and guiding personalised interventions. Global efforts to restore redox homeostasis have spurred development of targeted antioxidants, lifestyle modifications and pharmacological eNOS-recoupling agents, cementing oxidative stress as a central therapeutic focus in cardiovascular health.
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Oxidative Stress and Endothelial Function in Cardiovascular Health publication trend
The graph below shows the total number of articles in oxidative stress and endothelial function in cardiovascular health across all publications each year (not limited to Nature Index journals).
Technical terms
Oxidative stress: An imbalance between pro-oxidant species and antioxidant defences that disrupts redox signalling and damages cellular structures.
Endothelial dysfunction: A pathological state in which the endothelium loses its capacity to regulate vascular tone, barrier function and haemostasis, adopting a pro-inflammatory and pro-thrombotic phenotype.
Reactive oxygen species (ROS): Highly reactive molecules derived from oxygen metabolism, including superoxide and hydrogen peroxide, capable of oxidising lipids, proteins and nucleic acids.
Nitric oxide (NO) bioavailability: The effective concentration of NO available to mediate vasodilatation, inhibit platelet aggregation and suppress inflammation.
References
- The role of oxidative stress in diabetes mellitus-induced vascular endothelial dysfunction. Cardiovascular Diabetology (2023).
- Oxidative Stress-Induced Endothelial Dysfunction in Cardiovascular Diseases. Frontiers in Bioscience-Landmark (2022).
- Vascular Oxidative Stress: Impact and Therapeutic Approaches. Frontiers in Physiology (2018).
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