The Role of Iron in Atherosclerosis in Apolipoprotein E Deficient Mice

Frontiers in Cardiovascular Medicine

article

Juan Ma¹  Hui-Min Ma¹  Meng-Qi Shen¹  Yuan Yuan Wang²  Yu-Xin Bao⁴  Yong Liu⁵  Ya Ke⁶  Zhong-Ming Qian¹ 

[1] Institute of Translational and Precision Medicine, Nantong University;Laboratory of Neuropharmacology, Fudan University School of Pharmacy;National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University;Research Center for Medicine and Biology, Zunyi Medical University;Department of Pain and Rehabilitation, The Second Affiliated Hospital, The Army Medical University;School of Biomedical Sciences and Gerald Choa Neuroscience Center, Faculty of Medicine, The Chinese University of Hong Kong

关键词: atherosclerosis;    apolipoprotein E (ApoE);    iron transport and regulation;    reactive oxygen species (ROS);    iron-mediated atherosclerosis;   

DOI  :  10.3389/fcvm.2022.857933

学科分类：地球科学(综合)

来源: Frontiers

【 摘 要 】

The role of iron in atherosclerosis is still a controversial and unsolved issue. Here, we investigated serum iron, expression of iron regulatory, transport and storage proteins, pro-inflammatory chemokines and cytokines in ApoE –/– mice. We demonstrated that ApoE –/– induced atherosclerosis and an increase in iron contents, expression of transferrin receptor 1 (TfR1), iron regulatory proteins (IRPs), heme oxygenase 1 (HO1), cellular adhesion molecules and pro-inflammatory cytokines, production of reactive oxygen species (ROS), and a reduction in expression of superoxide dismutase and glutathione peroxidase enzyme in aortic tissues. All of these changes induced by ApoE deficiency could be significantly abolished by deferoxamine. The data showed that the increased iron in aortic tissues was mainly due to the increased iron uptake via IRP/TfR1 upregulation. These findings plus a brief analysis of the controversial results reported previously showed that ApoE deficiency-induced atherosclerosis is partly mediated by the increased iron in aortic tissues.

【 授权许可】

CC BY