Chemokine‐like factor 1 (CKLF1) aggravates neointimal hyperplasia through activating the NF‐κB /VCAM‐1 pathway | Zendy

Liu Xing | Zendy; Qu Chengjia | Zendy; Zhang Yongbao | Zendy; Fang Jie | Zendy; Teng Lequn | Zendy; Zhang Rujiao | Zendy; Zhang Xiangyu | Zendy; Shen Chenyang | Zendy

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Chemokine‐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.

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