The Role of ADAM17 in Inflammation-Related Atherosclerosis
Journal of Cardiovascular Translational Research, ISSN: 1937-5395, Vol: 15, Issue: 6, Page: 1283-1296
2022
- 8Citations
- 16Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations8
- Citation Indexes8
- CrossRef2
- Captures16
- Readers16
- 16
Review Description
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. Graphical abstract: ADAM17 promotes vascular inflammation in endothelial cells, smooth muscle cells, and macrophages, and regulates the occurrence and development of atherosclerosis.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85131334178&origin=inward; http://dx.doi.org/10.1007/s12265-022-10275-4; http://www.ncbi.nlm.nih.gov/pubmed/35648358; https://link.springer.com/10.1007/s12265-022-10275-4; https://dx.doi.org/10.1007/s12265-022-10275-4; https://link.springer.com/article/10.1007/s12265-022-10275-4
Springer Science and Business Media LLC
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