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Published on: May 6, 2014
The Role of ADAM17 in Inflammation-Related Atherosclerosis
Bai-Yi Tang1, Jin Ge1, Yang Wu2
1Department of Cardiology, Third Xiang-Ya Hospital, Central South University, 138 Tongzipo Road, Changsha, 410013, Hunan, China.
Insights
A disintegrin and metalloprotease 17 (ADAM17) promotes vascular inflammation, contributing to atherosclerosis development. Understanding ADAM17
Area of Science:
- Biochemistry
- Immunology
- Cardiovascular Research
Background:
- Atherosclerosis is a chronic inflammatory disease with poor prognosis and significant economic burden.
- A disintegrin and metalloprotease 17 (ADAM17) is a key enzyme involved in protein shedding and intracellular signaling.
- ADAM17-mediated inflammation is implicated in atherosclerosis, but its precise role is not fully understood.
Purpose of the Study:
- To review the activation, function, and regulation of ADAM17.
- To detail the role of ADAM17-mediated inflammatory damage in atherosclerosis pathogenesis.
- To discuss controversial aspects of ADAM17's involvement in atherosclerosis.
Main Methods:
- Literature review on ADAM17 activation, function, and regulation.
- Analysis of ADAM17's role in inflammatory processes within vascular cells.
- Synthesis of current knowledge on ADAM17 and atherosclerosis.
Main Results:
- ADAM17 promotes vascular inflammation in endothelial cells, smooth muscle cells, and macrophages.
- ADAM17 plays a regulatory role in the occurrence and development of atherosclerosis.
- The specific mechanisms linking ADAM17's diverse functions to atherosclerosis pathogenesis require further elucidation.
Conclusions:
- ADAM17 is a significant mediator of vascular inflammation contributing to atherosclerosis.
- Further insights into ADAM17 biology may facilitate rational management strategies for atherosclerosis.
- Targeting ADAM17 could offer a potential therapeutic avenue for preventing and treating atherosclerosis.
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.
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