Open AccessChemokine‐like factor 1 (CKLF1) aggravates neointimal hyperplasia through activating the NF‐κB /VCAM‐1 pathway
Author(s) -
Liu Xing,
Qu Chengjia,
Zhang Yongbao,
Fang Jie,
Teng Lequn,
Zhang Rujiao,
Zhang Xiangyu,
Shen Chenyang
Publication year - 2020
Publication title -
febs open bio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.718
H-Index - 31
ISSN - 2211-5463
DOI - 10.1002/2211-5463.12942
Subject(s) - vcam 1 , neointimal hyperplasia , downregulation and upregulation , chemokine , chemistry , nf κb , microbiology and biotechnology , cancer research , inflammation , adhesion , cell adhesion , restenosis , medicine , immunology , biology , biochemistry , stent , gene , organic chemistry
Neointimal hyperplasia (NIH) plays a pivotal role in vascular restenosis after revascularization. We previously identified that chemokine‐like factor 1 (CKLF1) could aggravate NIH by arresting smooth muscle cells in G2/M phase and preventing apoptosis via phosphoinositide 3‐kinase/AKT/nuclear factor‐kappa B signaling. Here, we demonstrate that CKLF1 promotes monocyte adhesion and smooth muscle cell migration via VCAM‐1. Our work furthers our understanding of how CKLF1 contributes to NIH causality.