Cardiovascular Inflammation and Lipid Metabolism Interactions

Cardiovascular disease remains the leading cause of morbidity and mortality worldwide, driven by metabolic and inflammatory disturbances. Central to disease initiation is the retention of atherogenic lipoproteins within the arterial wall, triggering endothelial activation and recruitment of monocytes, neutrophils and lymphocytes. Within the intima, monocytes differentiate into macrophages that ingest oxidised low-density lipoprotein, forming foam cells and secreting cytokines such as interleukin-1β and tumour necrosis factor-α. High-density lipoprotein mitigates these effects through reverse cholesterol transport, endothelial protection and modulation of leukocyte adhesion. Dysregulated lipid handling, oxidative modifications of lipoproteins and activation of inflammasomes promote necrotic core formation and fibrous cap thinning, predisposing to plaque rupture and thrombosis. Advances in lipidomics, immunophenotyping and imaging have revealed heterogeneous plaque microenvironments and patient-specific inflammatory signatures. Translational research targeting lipid–inflammatory axes, exemplified by statin therapy, PCSK9 inhibition and anti-interleukin-1β approaches, has demonstrated clinical benefit. Future strategies harnessing the interplay between lipid metabolism and immune regulation hold promise for precision prevention and therapy.

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Cardiovascular Inflammation and Lipid Metabolism Interactions publication trend

The graph below shows the total number of articles in cardiovascular inflammation and lipid metabolism interactions across all publications each year (not limited to Nature Index journals).

Technical terms

Atherosclerosis: A chronic vascular disease characterised by accumulation of lipids and inflammatory cells within the arterial intima, leading to plaque formation and vessel narrowing.

Foam cell: A lipid-engorged macrophage or other phagocyte that arises from uptake of modified lipoproteins, contributing to plaque growth and instability.

Neutrophil-to-HDL ratio (NHR): A composite biomarker calculated by dividing circulating neutrophil count by HDL cholesterol concentration, reflecting the balance between inflammation and lipid-mediated protective pathways.

Cholesteryl ester transfer protein (CETP): A plasma glycoprotein that transfers cholesteryl esters from HDL to apolipoprotein B-containing lipoproteins, influencing cholesterol distribution and immune cell function.

References

1. Neutrophil-to-High-Density Lipoprotein Ratio (NHR) and Neutrophil-to-Lymphocyte Ratio (NLR) as prognostic biomarkers for incident cardiovascular disease and all-cause mortality: A comparison study. American Journal of Preventive Cardiology (2024).
2. Giant phagocytes (Gφ) and neutrophil-macrophage hybrids in human carotid atherosclerotic plaques – An activated phenotype. Frontiers in Immunology (2023).
3. CETP Expression in Bone-Marrow-Derived Cells Reduces the Inflammatory Features of Atherosclerosis in Hypercholesterolemic Mice. Biomolecules (2023).