Oxidative Stress and Phospholipid Dynamics in Vascular Biology
Summary
Oxidative stress arises when an excess of reactive oxygen species (ROS) overwhelms cellular antioxidant defences, initiating lipid peroxidation and the generation of oxidised phospholipid species. In the vasculature, this process modifies the composition and biophysical properties of endothelial and plasma membranes, alters phospholipid turnover and engages a suite of receptors and enzymes. Oxidised phospholipids act as danger signals that modulate endothelial barrier function, leukocyte recruitment, platelet activation and smooth muscle cell behaviour. Key receptors such as cluster of differentiation 36 (CD36) recognise specific oxidised phospholipid motifs, triggering inflammatory cascades and foam cell formation in atherogenesis. Concurrently, enzymatic systems including phospholipases A₂ dynamically remodel oxidised lipids, influencing membrane fluidity, vesicle formation and local mediator release. The interplay between ROS generation, phospholipid oxidation and enzymatic processing contributes to endothelial dysfunction, thrombosis and vascular inflammation. Understanding these pathways has underpinned efforts to target receptor–ligand interactions, modulate phospholipase activity and enhance antioxidant capacity as therapeutic strategies in cardiovascular disease and related inflammatory disorders.
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Oxidative Stress and Phospholipid Dynamics in Vascular Biology publication trend
The graph below shows the total number of articles in oxidative stress and phospholipid dynamics in vascular biology across all publications each year (not limited to Nature Index journals).
Technical terms
Oxidative stress: An imbalance favouring ROS over antioxidants, leading to molecular damage.
Reactive oxygen species (ROS): Chemically reactive molecules derived from oxygen that can oxidise lipids and proteins.
Oxidised phospholipids (OxPL): Phospholipids modified by ROS, generating bioactive species that trigger receptor-mediated responses.
Phospholipase A₂ (PLA₂): Enzymes that hydrolyse the sn-2 acyl bond of phospholipids, crucial for membrane remodelling and mediator generation.
Cluster of differentiation 36 (CD36): A scavenger receptor that binds specific oxidised phospholipid species, mediating inflammatory and atherogenic processes.
References
- Aging-Related Accumulation of Truncated Oxidized Phospholipids Augments Infectious Lung Injury and Endothelial Dysfunction via Cluster of Differentiation 36-Dependent Mechanism. Cells (2023).
- Pharmacological heat-shock protein inducers and chemical chaperones inhibit upregulation of interleukin-8 by oxidized phospholipids. Inflammopharmacology (2023).
- Impact of Truncated Oxidized Phosphatidylcholines on Phospholipase A2 Activity in Mono- and Polyunsaturated Biomimetic Vesicles. International Journal of Molecular Sciences (2023).
- A Novel Family of Atherogenic Oxidized Phospholipids Promotes Macrophage Foam Cell Formation via the Scavenger Receptor CD36 and Is Enriched in Atherosclerotic Lesions*. Journal of Biological Chemistry (2002).
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