Oxidative Stress in Cardiovascular Pathophysiology
Summary
Oxidative stress describes the imbalance between the generation of reactive oxygen species (ROS) and the capacity of antioxidant defences to neutralise them. In the vascular system, excess ROS impairs endothelial function by reducing nitric oxide (NO) bioavailability, promoting inflammation and oxidising lipids, which collectively drive atherogenesis. Within arterial walls, ROS-mediated damage to proteins, lipids and DNA accelerates plaque initiation and vulnerability, while in myocardial tissue redox imbalance contributes to ischaemic injury and adverse remodelling. Antioxidant systems—including superoxide dismutases, catalase and glutathione peroxidases—normally maintain redox homeostasis, but become overwhelmed in hypertension, diabetes and dyslipidaemia. Understanding the cellular sources of ROS, the interplay with inflammatory signalling and the impact on vascular tone has informed a range of therapeutic strategies. These encompass pharmacological antioxidants, gene-based enhancement of endogenous enzymes and novel nano-engineered materials designed to modulate redox signalling. Globally, elucidating oxidative mechanisms is central to preventing cardiovascular morbidity and mortality and to developing precision interventions against atherothrombosis, heart failure and vascular complications of metabolic disease.
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Oxidative Stress in Cardiovascular Pathophysiology publication trend
The graph below shows the total number of articles in oxidative stress in cardiovascular pathophysiology across all publications each year (not limited to Nature Index journals).
Technical terms
Reactive Oxygen Species (ROS): Highly reactive oxygen-derived molecules, including superoxide and hydrogen peroxide, that can damage cellular structures when unregulated.
Endothelial Nitric Oxide Synthase (eNOS): An enzyme in endothelial cells responsible for producing NO, a critical regulator of vascular tone and inhibitor of thrombosis.
Nanoceria: Cerium oxide nanoparticles with redox activity that mimic antioxidant enzymes and, in some cases, generate NO.
Caveolin-1: A membrane scaffold protein that binds eNOS and controls its activation and localisation in endothelial cells.
Atherogenesis: The process of arterial plaque formation characterised by lipid accumulation, chronic inflammation and fibrous cap development.
References
- NOS-like activity of CeO2 nanozymes contributes to diminishing the vascular plaques. Journal of Nanobiotechnology (2024).
- Deficiency of neutral cholesterol ester hydrolase 1 (NCEH1) impairs endothelial function in diet-induced diabetic mice. Cardiovascular Diabetology (2024).
- ROS-Induced Endothelial Dysfunction in the Pathogenesis of Atherosclerosis. Aging and Disease (2024).
- Oxidative Stress-Mediated Atherosclerosis: Mechanisms and Therapies. Frontiers in Physiology (2017).
- Redox Roles of Reactive Oxygen Species in Cardiovascular Diseases. International Journal of Molecular Sciences (2015).
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