Oxidative Stress Mechanisms in Cardiovascular Disease
Summary
Oxidative stress represents a fundamental disturbance in redox homeostasis, arising when the generation of reactive oxygen species (ROS) overwhelms endogenous antioxidant defences. In the vasculature, excessive ROS originate from mitochondrial respiration, NADPH oxidases, uncoupled nitric oxide synthase and xanthine oxidase, among other sources. These oxidants inflict damage on lipids, proteins and DNA, provoking endothelial dysfunction, vascular inflammation and smooth muscle cell proliferation. As a result, the endothelium loses its capacity to regulate vascular tone and barrier function, nitric oxide bioavailability falls and pro-thrombotic pathways are engaged. Oxidative modifications of low-density lipoprotein (LDL) promote its uptake by macrophages, driving foam cell formation and atheroma development. In the myocardium, reperfusion injury and maladaptive remodelling are exacerbated by redox imbalance, with ROS-mediated signalling triggering hypertrophy and apoptosis. Counter-regulatory systems—including superoxide dismutases, catalase, glutathione peroxidases and peroxiredoxins—work in concert to neutralise ROS, yet chronic risk factors such as hypertension, diabetes, smoking and ageing erode these defences. Understanding these pathways has guided the exploration of targeted antioxidant therapies, dietary interventions and pharmacological agents aimed at restoring redox balance and protecting cardiovascular health.
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Oxidative Stress Mechanisms in Cardiovascular Disease publication trend
The graph below shows the total number of articles in oxidative stress mechanisms in cardiovascular disease across all publications each year (not limited to Nature Index journals).
Technical terms
Reactive oxygen species (ROS): Highly reactive oxygen-derived molecules capable of oxidising cellular macromolecules.
Oxidative stress: A state in which ROS production exceeds antioxidant capacity, leading to cellular injury.
Endothelial dysfunction: Impaired vasodilatory, anti-inflammatory and antithrombotic functions of the vascular lining.
Foam cells: Lipid-laden macrophages formed through uptake of oxidised low-density lipoprotein, central to plaque formation.
NADPH oxidase: A multi-subunit enzyme complex that produces superoxide as part of physiological and pathological signalling.
References
- Targeting oxidative stress as a preventive and therapeutic approach for cardiovascular disease. Journal of Translational Medicine (2023).
- Attenuating lipid metabolism in atherosclerosis: The potential role of Anti-oxidative effects on low-density lipoprotein of herbal medicines. Frontiers in Pharmacology (2023).
- Oxidative Stress in Human Atherothrombosis: Sources, Markers and Therapeutic Targets. International Journal of Molecular Sciences (2017).
- Oxidative Stress in Cardiovascular Diseases: Still a Therapeutic Target?. Nutrients (2019).
- Biomarkers of Oxidative Stress Tethered to Cardiovascular Diseases. Oxidative Medicine and Cellular Longevity (2022).
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