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Review

Emerging Roles of Tumor Necrosis Factor-Stimulated Gene-6 in the Pathophysiology and Treatment of Atherosclerosis

1
Laboratory of Cardiovascular Medicine, Tokyo University of Pharmacy and Life Sciences, 1432-1 Horinouchi, Hachioji-City, Tokyo 192-0392, Japan
2
Division of Cardiology, Department of Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8666, Japan
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2018, 19(2), 465; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms19020465
Received: 21 December 2017 / Revised: 22 January 2018 / Accepted: 30 January 2018 / Published: 5 February 2018
(This article belongs to the Special Issue Pathomechanisms of Atherosclerosis. Part I)
Tumor necrosis factor-stimulated gene-6 (TSG-6) is a 35-kDa glycoprotein that has been shown to exert anti-inflammatory effects in experimental models of arthritis, acute myocardial infarction, and acute cerebral infarction. Several lines of evidence have shed light on the pathophysiological roles of TSG-6 in atherosclerosis. TSG-6 suppresses inflammatory responses of endothelial cells, neutrophils, and macrophages as well as macrophage foam cell formation and vascular smooth muscle cell (VSMC) migration and proliferation. Exogenous TSG-6 infusion and endogenous TSG-6 attenuation with a neutralizing antibody for four weeks retards and accelerates, respectively, the development of aortic atherosclerotic lesions in ApoE-deficient mice. TSG-6 also decreases the macrophage/VSMC ratio (a marker of plaque instability) and promotes collagen fibers in atheromatous plaques. In patients with coronary artery disease (CAD), plasma TSG-6 levels are increased and TSG-6 is abundantly expressed in the fibrous cap within coronary atheromatous plaques, indicating that TSG-6 increases to counteract the progression of atherosclerosis and stabilize the plaque. These findings indicate that endogenous TSG-6 enhancement and exogenous TSG-6 replacement treatments are expected to emerge as new lines of therapy against atherosclerosis and related CAD. Therefore, this review provides support for the clinical utility of TSG-6 in the diagnosis and treatment of atherosclerotic cardiovascular diseases. View Full-Text
Keywords: TSG-6; atherosclerosis; endothelial cell; macrophage; vascular smooth muscle cell; coronary artery disease TSG-6; atherosclerosis; endothelial cell; macrophage; vascular smooth muscle cell; coronary artery disease
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MDPI and ACS Style

Watanabe, R.; Sato, Y.; Ozawa, N.; Takahashi, Y.; Koba, S.; Watanabe, T. Emerging Roles of Tumor Necrosis Factor-Stimulated Gene-6 in the Pathophysiology and Treatment of Atherosclerosis. Int. J. Mol. Sci. 2018, 19, 465. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms19020465

AMA Style

Watanabe R, Sato Y, Ozawa N, Takahashi Y, Koba S, Watanabe T. Emerging Roles of Tumor Necrosis Factor-Stimulated Gene-6 in the Pathophysiology and Treatment of Atherosclerosis. International Journal of Molecular Sciences. 2018; 19(2):465. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms19020465

Chicago/Turabian Style

Watanabe, Rena, Yuki Sato, Nana Ozawa, Yui Takahashi, Shinji Koba, and Takuya Watanabe. 2018. "Emerging Roles of Tumor Necrosis Factor-Stimulated Gene-6 in the Pathophysiology and Treatment of Atherosclerosis" International Journal of Molecular Sciences 19, no. 2: 465. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms19020465

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