Atherosclerosis and Toll-Like Receptor4 (TLR4), Lectin-Like Oxidized Low-Density Lipoprotein-1 (LOX-1), and Proprotein Convertase Subtilisin/Kexin Type9 (PCSK9)

Author:

Bagheri Bahador12ORCID,Khatibiyan Feyzabadi Zahra3ORCID,Nouri Ahmad3ORCID,Azadfallah Ali3ORCID,Mahdizade Ari Mahyar3ORCID,Hemmati Maral1ORCID,Darban Mahboubeh4ORCID,Alavi Toosi Parisa3ORCID,Banihashemian Seyedeh Zahra3ORCID

Affiliation:

1. Cancer Research Center, Semnan University of Medical Sciences, Semnan, Iran

2. Center for Molecular Cardiology, University of Zurich, Schlieren, Switzerland

3. Student Research Committee, Faculty of Medicine, Semnan University of Medical Sciences, Semnan, Iran

4. Department of Internal Medicine, Kowsar Hospital, Semnan University of Medical Sciences, Semnan, Iran

Abstract

Atherosclerosis is a leading cause of death in the world. A significant body of evidence suggests that inflammation and various players are implicated and have pivotal roles in the formation of atherosclerotic plaques. Toll-like receptor 4 (TLR4) is linked with different stages of atherosclerosis. This receptor is highly expressed in the endothelial cells (ECs) and atherosclerotic plaques. TLR4 activation can lead to the production of inflammatory cytokines and related responses. Lectin-like oxidized low-density lipoprotein-1 (LOX-1), an integral membrane glycoprotein with widespread expression on the ECs, is involved in atherosclerosis and has some common pathways with TLR4 in atherosclerotic lesions. In addition, proprotein convertase subtilisin/kexin type9 (PCSK9), which is a regulatory enzyme with different roles in cholesterol uptake, is implicated in atherosclerosis. At present, TLR4, PCSK9, and LOX-1 are increasingly acknowledged as key players in the pathogenesis of atherosclerotic cardiovascular diseases. Herein, we presented the current evidence on the structure, functions, and roles of TLR4, PCSK9, and LOX-1 in atherosclerosis.

Funder

European Society Of Cardiology

Publisher

Hindawi Limited

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