The role of tumor necrosis factor-like weak inducer of apoptosis in atherosclerosis via its two different receptors

Hengdao Liu; Dan Lin; Hong Xiang; Wei Chen; Shaoli Zhao; Hui Peng; Jie Yang; Pan Chen; Shuhua Chen; Hongwei Lu

doi:10.3892/etm.2017.4600

The role of tumor necrosis factor-like weak inducer of apoptosis in atherosclerosis via its two different receptors

Exp Ther Med. 2017 Aug;14(2):891-897. doi: 10.3892/etm.2017.4600. Epub 2017 Jun 14.

Authors

Hengdao Liu^{1

2}, Dan Lin³, Hong Xiang¹, Wei Chen¹, Shaoli Zhao^{1

4}, Hui Peng¹, Jie Yang¹, Pan Chen¹, Shuhua Chen¹, Hongwei Lu^{1

2}

Affiliations

¹ Center for Experimental Medical Research, The Third Xiangya Hospital of Central South University, Changsha, Hunan 410013, P.R. China.
² Department of Cardiology, The Third Xiangya Hospital of Central South University, Changsha, Hunan 410013, P.R. China.
³ Qingdao Center for Disease Control and Prevention, Qingdao, Shandong 266033, P.R. China.
⁴ Department of Endocrinology, The Third Xiangya Hospital of Central South University, Changsha, Hunan 410013, P.R. China.

Abstract

At present, it is commonly accepted that atherosclerosis is a chronic inflammatory disease characterized by disorder of the arterial wall. As one of the inflammatory cytokines of the tumor necrosis factor superfamily, tumor necrosis factor-like weak inducer of apoptosis (TWEAK) participates in the formation and progression of atherosclerosis. TWEAK, when binding to its initial receptor, fibroblast growth factor inducible molecule 14 (Fn14), exerts adverse biological functions in atherosclerosis, including dysfunction of endothelial cells, phenotypic change of smooth muscle cells and inflammatory responses of monocytes/macrophages. However, accumulating data supports that, besides Fn14, TWEAK also binds to cluster of differentiation (CD)163, an anti-inflammatory cytokine and a scavenger receptor exclusively expressed by monocytes and macrophages. Furthermore, it has been demonstrated that CD163 is able to internalize TWEAK and likely elicits protective effects in atherosclerosis by terminating inflammation induced by TWEAK. In the present study, the role of TWEAK in atherosclerosis was reviewed, with a predominant focus on CD163 and Fn14 receptors.

Keywords: atherosclerosis; cluster of differentiation 163; fibroblast growth factor inducible molecule 14; receptor; tumor necrosis factor-like weak inducer of apoptosis.