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Updated: Jun 27, 2026

Programming Stem Cells for Therapeutic Angiogenesis Using Biodegradable Polymeric Nanoparticles

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Published on: September 27, 2013

Targeted Atherosclerosis Treatment Using Vascular Cell Adhesion Molecule-1 Targeting Peptide-Engineered Plant-Derived

Chanwoo Choi¹, Won Jong Rhee^1,2,3

¹Department of Bioengineering and Nano-Bioengineering, Incheon National University, Incheon 22012, Republic of Korea.

International Journal of Molecular Sciences

|September 27, 2025

Summary

Onion-derived nanovesicles (Onex) engineered with VHPK peptide (V-Onex) target inflamed cells. This novel therapy effectively reduces inflammation and key processes in atherosclerosis, offering a promising new treatment approach.

Keywords:

VCAM-1 VHPK peptide atherosclerosis extracellular vesicle onion

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Published on: June 20, 2025

Area of Science:

Biomedical Engineering
Nanotechnology
Cardiovascular Research

Background:

Atherosclerosis is a complex vascular disease driven by inflammation and lipid accumulation, leading to heart attack and stroke.
Current treatments for atherosclerosis focus on cholesterol reduction or anticoagulation, failing to address its multifactorial nature.
There is a need for innovative therapies that target the dynamic pathological processes of atherosclerosis.

Purpose of the Study:

To develop and evaluate a novel targeted nanovesicle platform, V-Onex, for atherosclerosis therapy.
To engineer onion-derived extracellular vesicles (Onex) with a VHPK peptide for specific targeting of inflamed endothelial cells.
To assess the therapeutic potential of V-Onex in modulating key inflammatory and cellular processes in atherosclerosis.

Main Methods:

Onion-derived extracellular vesicles (Onex) were engineered with the VHPK peptide to create V-Onex, targeting vascular cell adhesion molecule-1 (VCAM-1).
Biocompatibility and cytotoxicity were evaluated in human umbilical vein endothelial cells (HUVECs) and THP-1 cells.
The efficacy of V-Onex was assessed by measuring its accumulation in inflamed cells, reduction of inflammatory markers, and inhibition of monocyte-endothelial cell interactions and foam cell formation.

Main Results:

Engineered V-Onex demonstrated excellent biocompatibility and stability without cytotoxicity.
V-Onex selectively accumulated in inflamed endothelial cells, significantly reducing inflammatory markers.
V-Onex suppressed endothelial cell migration, reduced monocyte adhesion, inhibited oxidized LDL uptake, and decreased foam cell formation.

Conclusions:

V-Onex represents a promising modular targeted nanovesicle platform for atherosclerosis.
This engineered nanovesicle effectively modulates multiple pathological processes involved in atherosclerotic progression.
V-Onex holds potential as a novel therapeutic strategy for treating atherosclerosis.