# Overstretch causes lipid accumulation in vascular smooth muscle cells dependent on NADPH oxidase 1

## TL;DR

This study shows that stretching vascular smooth muscle cells increases lipid accumulation, a key step in atherosclerosis, through a mechanism involving the NOX1 protein.

## Contribution

The paper identifies NOX1 as a novel mediator of lipid accumulation in vascular smooth muscle cells under mechanical stretch.

## Key findings

- Cyclic stretching of vascular smooth muscle cells increases intracellular lipid accumulation.
- NOX1 upregulation under stretch is linked to the JAK/STAT signaling pathway.
- Inhibiting NOX1 or reactive oxygen species reduces lipid accumulation in these cells.

## Abstract

At the bend and bifurcation of arteries prone to atherosclerosis, pulsatile blood retention may cause overstretch on the tube wall. It has been reported that more than half of the foam cells found in atherosclerotic plaques are derived from vascular smooth muscle cells (VSMCs), but the mechanism is not adequately understood. In this work, we used a microfluidic device to apply a cyclic stretch (15 ​% and 0.05 ​Hz) on the VSMC for 24 ​h. The stretch caused a significant increase in the intracellular lipid accumulation, accompanying with the increased NOX1 and CD36 protein expression. On the other hand, inhibition of NOX1 activity, elimination of reactive oxygen species (ROS), or knockdown of NOX1 expression could significantly inhibit intracellular lipid accumulation. In addition, the NOX1 upregulation caused by 15 ​% stretch was related to the JAK/STAT signaling pathway. Our results reveal a novel mechanism of VSMC foam cell formation caused by the upregulation of NOX1.

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