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Review
. 2022 Dec;15(6):1283-1296.
doi: 10.1007/s12265-022-10275-4. Epub 2022 Jun 1.

The Role of ADAM17 in Inflammation-Related Atherosclerosis

Bai-Yi Tang #  1 , Jin Ge #  1 , Yang Wu  2 , Juan Wen  3 , Xiao-Hong Tang  4
Affiliations
Review

The Role of ADAM17 in Inflammation-Related Atherosclerosis

Bai-Yi Tang et al. J Cardiovasc Transl Res. 2022 Dec.

Abstract

Atherosclerosis is a chronic inflammatory disease that poses a huge economic burden due to its extremely poor prognosis. Therefore, it is necessary to explore potential mechanisms to improve the prevention and treatment of atherosclerosis. A disintegrin and metalloprotease 17 (ADAM17) is a cell membrane-bound protein that performs a range of functions through membrane protein shedding and intracellular signaling. ADAM17-mediated inflammation has been identified to be an important contributor to atherosclerosis; however, the specific relationship between its multiple regulatory roles and the pathogenesis of atherosclerosis remains unclear. Here, we reviewed the activation, function, and regulation of ADAM17, described in detail the role of ADAM17-mediated inflammatory damage in atherosclerosis, and discussed several controversial points. We hope that these insights into ADAM17 biology will lead to rational management of atherosclerosis. ADAM17 promotes vascular inflammation in endothelial cells, smooth muscle cells, and macrophages, and regulates the occurrence and development of atherosclerosis.

Keywords: A disintegrin and metalloprotease 17; Atherosclerosis; Inflammation; Vascular biology.

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References

    1. Wei, S., Wang, H., Zhang, G., Lu, Y., An, X., Ren, S., Wang, Y., Chen, Y., White, J. G., Zhang, C., et al. (2013). Platelet IκB kinase-β deficiency increases mouse arterial neointima formation via delayed glycoprotein Ibα shedding. Arteriosclerosis, Thrombosis, and Vascular Biology, 33, 241–248. https://doi.org/10.1161/ATVBAHA.112.300781 - DOI
    1. Zhang, Y., Wang, Y., Zhou, D., Zhang, L. S., Deng, F. X., Shu, S., Wang, L. J., Wu, Y., Guo, N., Zhou, J., & Yuan, Z. Y. (2019). Angiotensin II deteriorates advanced atherosclerosis by promoting MerTK cleavage and impairing efferocytosis through the AT(1)R/ROS/p38 MAPK/ADAM17 pathway. American Journal of Physiology-Cell Physiology, 317, C776-C787. https://doi.org/10.1152/ajpcell.00145.2019 - DOI
    1. Couchie, D., Vaisman, B., Abderrazak, A., Mahmood, D. F. D., Hamza, M. M., Canesi, F., Diderot, V., El Hadri, K., Nègre-Salvayre, A., Le Page, A., et al. (2017). Human plasma Thioredoxin-80 increases with age and in ApoE(-/-) mice induces inflammation, angiogenesis, and atherosclerosis. Circulation, 136, 464–475. https://doi.org/10.1161/CIRCULATIONAHA.117.027612 - DOI
    1. Gooz, M. (2010). ADAM-17: The enzyme that does it all. Critical Reviews in Biochemistry and Molecular Biology, 45, 146–169. https://doi.org/10.3109/10409231003628015 - DOI
    1. Donners, M. M., Wolfs, I. M., Olieslagers, S., Mohammadi-Motahhari, Z., Tchaikovski, V., Heeneman, S., van Buul, J. D., Caolo, V., Molin, D. G., Post, M. J., & Waltenberger, J. (2010). A disintegrin and metalloprotease 10 is a novel mediator of vascular endothelial growth factor-induced endothelial cell function in angiogenesis and is associated with atherosclerosis. Arteriosclerosis, Thrombosis, and Vascular Biology, 30, 2188–2195. https://doi.org/10.1161/ATVBAHA.110.213124 - DOI

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