Cathepsin K contributed to disturbed flow-induced atherosclerosis is dependent on integrin-actin cytoskeleton–NF–κB pathway

Fei Fang; Tang Feng; Jianwei Li; Huaiyi Zhang; Qin Wang; Yidan Chen; Guixue Wang; Yang Shen; Xiaoheng Liu

doi:10.1016/j.gendis.2022.03.020

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Cathepsin K contributed to disturbed flow-induced atherosclerosis is dependent on integrin-actin cytoskeleton–NF–κB pathway

Full-length article | 更新时间：2023-05-16

- Cathepsin K contributed to disturbed flow-induced atherosclerosis is dependent on integrin-actin cytoskeleton–NF–κB pathway
- Cathepsin K contributed to disturbed flow-induced atherosclerosis is dependent on integrin-actin cytoskeleton–NF–κB pathway
- Genes & Diseases 2023年10卷第2期
- 作者机构：
  
  1. Key Laboratory for Biorheological Science and Technology of Ministry of Education, State and Local Joint Engineering Laboratory for Vascular Implants, College of Bioengineering, Chongqing University,Chongqing,China,400030
  2. Institute of Biomedical Engineering, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University,Sichuan,Chengdu,China,610041
  3. Department of Endocrinology and Metabolism, West China Hospital, Sichuan University,Sichuan,Chengdu,China,610041
- 作者简介：
- 基金信息：
- DOI：10.1016/j.gendis.2022.03.020
  中图分类号：
- 纸质出版日期：2023，
  
  网络出版日期：2023-3-1，
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Cathepsin K contributed to disturbed flow-induced atherosclerosis is dependent on integrin-actin cytoskeleton–NF–κB pathway[J]. Genes & Diseases, 2023,10(2).

Fei Fang, Tang Feng, Jianwei Li, et al. Cathepsin K contributed to disturbed flow-induced atherosclerosis is dependent on integrin-actin cytoskeleton–NF–κB pathway[J]. Genes & Diseases, 2023,10(2).
Cathepsin K contributed to disturbed flow-induced atherosclerosis is dependent on integrin-actin cytoskeleton–NF–κB pathway[J]. Genes & Diseases, 2023,10(2). DOI： 10.1016/j.gendis.2022.03.020.

Fei Fang, Tang Feng, Jianwei Li, et al. Cathepsin K contributed to disturbed flow-induced atherosclerosis is dependent on integrin-actin cytoskeleton–NF–κB pathway[J]. Genes & Diseases, 2023,10(2). DOI： 10.1016/j.gendis.2022.03.020.

摘要

Abstract

herosclerosis is a chronic inflammatory disease

occurring preferentially in bifurcation

branching

and bending of blood vessels exposed to disturbed flow. Disturbed flow in atheroprone areas activates elevated proteases

degrading elastin lamellae and collagenous matrix

resulting in endothelial dysfunction and vascular remodeling. As a mediator for extracellular matrix protein degradation

cathepsin K (CTSK) was directly regulated by hemodynamics and contributed to atherosclerosis. The mechanism of CTSK responding to disturbed flow and contributing to disturbed flow-induced atherosclerosis is unclear. In this study

the partial carotid ligation model of mice and

in vitro

disturbed shear stress model were constructed to explore the contribution and potential mechanism of CTSK in atherosclerosis. Our results indicated that CTSK elevated in the disturbed flow area

in vivo

and

in vitro

along with endothelial inflammation and atherogenesis. Additionally

the expression of integrin αvβ3 was upregulated in these atheroprone areas. We found that inhibition of the integrin αvβ3-cytoskeleton pathway could significantly block the activation of NF-κB and the expression of CTSK. Collectively

our findings unraveled that disturbed flow induces increased CTSK expression

and contributes to endothelial inflammation and vascular remodeling

leading to atherogenesis eventually. This study is helpful to provide new enlightenment for the therapy of atherosclerosis.

关键词

Keywords

AtherosclerosisCathepsin KDisturbed flowIntegrinNF-κB

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