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

Mechanobiology in Medicine Pub Date : 2025-03-26 DOI:10.1016/j.mbm.2025.100129

Jiazhen Zhang , Qinfen Li , Suoqi Ding , Wei Xu , Jilei Su , Jingang Cui , Yongsheng Ding

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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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过度拉伸引起血管平滑肌细胞依赖于NADPH氧化酶1的脂质积累

在动脉易发生动脉粥样硬化的弯曲和分叉处，搏动性血液潴留可能导致管壁过度拉伸。据报道，在动脉粥样硬化斑块中发现的泡沫细胞中有一半以上来自血管平滑肌细胞（VSMCs），但其机制尚不清楚。在这项工作中，我们使用微流体装置在VSMC上施加循环拉伸（15%和0.05 Hz） 24小时。拉伸引起细胞内脂质积累显著增加，并伴有NOX1和CD36蛋白表达增加。另一方面，抑制NOX1活性、消除活性氧（ROS）或敲低NOX1表达可显著抑制细胞内脂质积累。此外，15%拉伸引起的NOX1上调与JAK/STAT信号通路有关。我们的研究结果揭示了一种由NOX1上调引起的VSMC泡沫细胞形成的新机制。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Mechanobiology in Medicine

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