Atherogenic Mechanisms and Lipoprotein Interaction in Vascular Diseases

Atherogenesis arises from a complex interplay between circulating lipoproteins, vascular cells and immune mediators leading to plaque formation within arterial walls. Low-density lipoprotein (LDL) particles infiltrate the subendothelial space where they undergo biochemical modifications such as oxidation and desialylation. These altered lipoproteins are avidly taken up by macrophages, giving rise to lipid-laden foam cells that constitute the core of evolving lesions. Endothelial dysfunction, triggered by disturbed shear stress, hypertension or metabolic insults, precedes lipid deposition and promotes adhesion molecule expression, facilitating mononuclear cell recruitment. Smooth muscle cells migrate and proliferate in response to cytokines and growth factors, contributing to fibrous cap formation and plaque stability. High-density lipoprotein (HDL) exerts anti-atherogenic effects through reverse cholesterol transport and antioxidant enzyme carriage, although functionality may be compromised under chronic inflammation. Emerging regulators include non-coding RNAs, epigenetic modifications and enzymatic pathways that alter lipoprotein structure and immunogenicity. Collectively, these processes culminate in a dynamic lesion that may rupture or calcify, underpinning clinical events such as myocardial infarction and stroke. Understanding the molecular crosstalk between lipoproteins and vascular cells has informed the development of diagnostic biomarkers and targeted therapies aimed at modulating lipid handling, inflammatory responses and endothelial health.

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Atherogenic Mechanisms and Lipoprotein Interaction in Vascular Diseases publication trend

The graph below shows the total number of articles in atherogenic mechanisms and lipoprotein interaction in vascular diseases across all publications each year (not limited to Nature Index journals).

Technical terms

Atherogenesis: The multi-step process by which fatty streaks and plaques develop in arterial walls through lipid deposition and inflammation.

Endothelial dysfunction: Impaired vasodilatory and barrier functions of the endothelium that promote vascular inflammation and permeability.

Low-density lipoprotein (LDL): A class of lipoproteins responsible for cholesterol transport from the liver to peripheral tissues, prone to atherogenic modification.

Foam cell: A lipid-filled macrophage or smooth muscle cell within the arterial intima that contributes to plaque growth.

Desialylation: The enzymatic removal of sialic acid residues from glycoproteins or lipoproteins, altering their clearance and receptor interactions.

Oxidised LDL: LDL particles that have undergone oxidative modification, increasing their uptake by scavenger receptors and pro-inflammatory potential.

MicroRNA: A small non-coding RNA molecule that regulates gene expression post-transcriptionally, influencing lipid metabolism and vascular cell function.

References

1. MicroRNAs Regulate Function in Atherosclerosis and Clinical Implications. Oxidative Medicine and Cellular Longevity (2023).
2. DHX9 Strengthens Atherosclerosis Progression By Promoting Inflammation in Macrophages. Inflammation (2023).
3. Proatherogenic Sialidases and Desialylated Lipoproteins: 35 Years of Research and Current State from Bench to Bedside. Biomedicines (2021).