{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T16:08:09Z","timestamp":1791043689809,"version":"4.1.0"},"reference-count":75,"publisher":"Oxford University Press (OUP)","issue":"11","license":[{"start":{"date-parts":[[2020,3,20]],"date-time":"2020-03-20T00:00:00Z","timestamp":1584662400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"name":"Lin Huddleston National Heart Foundation Senior Fellowship"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2021,9,28]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>While the advent of drug-eluting stents has been clinically effective in substantially reducing the rates of major stent-related adverse events compared with bare metal stents, vascular biological problems such as neointimal hyperplasia, delayed re-endothelialization, late stent thrombosis are not eliminated and, increasingly, neoatherosclerosis is the underlying mechanism for very late stent failure. Further understanding regarding the mechanisms underlying the biological responses to stent deployment is therefore required so that new and improved therapies can be developed. This review will discuss the accumulating evidence that the chemokines, small inflammatory proteins, play a role in each key biological process of stent biocompatibility. It will address the chemokine system in its specialized roles in regulating the multiple facets of vascular biocompatibility including neointimal hyperplasia, endothelial progenitor cell (EPC) mobilization and re-endothelialization after vascular injury, platelet activation and thrombosis, as well as neoatherosclerosis. The evidence in this review suggests that chemokine-targeting strategies may be effective in controlling the pathobiological processes that lead to stent failure. Preclinical studies provide evidence that inhibition of specific chemokines and\/or broad-spectrum inhibition of the CC-chemokine class prevents neointimal hyperplasia, reduces thrombosis and suppresses the development of neoatherosclerosis. In contrast, however, to these apparent deleterious effects of chemokines on stent biocompatibility, the CXC chemokine, CXCL12, is essential for the mobilization and recruitment of EPCs that make important contributions to re-endothelialization post-stent deployment. This suggests that future chemokine inhibition strategies would need to be correctly targeted so that all key stent biocompatibility areas could be addressed, without compromising important adaptive biological responses.<\/jats:p>","DOI":"10.1093\/cvr\/cvaa072","type":"journal-article","created":{"date-parts":[[2020,3,18]],"date-time":"2020-03-18T13:51:03Z","timestamp":1584539463000},"page":"2299-2308","source":"Crossref","is-referenced-by-count":8,"title":["The multiple roles of chemokines in the mechanisms of stent biocompatibility"],"prefix":"10.1093","volume":"117","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9400-6088","authenticated-orcid":false,"given":"Dhanya","family":"Ravindran","sequence":"first","affiliation":[{"name":"Heart Research Institute, Sydney 2042, Australia"},{"name":"The University of Sydney, Sydney Medical School, Sydney 2006, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keyvan","family":"Karimi Galougahi","sequence":"additional","affiliation":[{"name":"The University of Sydney, Sydney Medical School, Sydney 2006, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1875-4882","authenticated-orcid":false,"given":"Joanne T M","family":"Tan","sequence":"additional","affiliation":[{"name":"South Australian Health and Medical Research Institute, Vascular Research Centre, Adelaide 5000, Australia"},{"name":"University of Adelaide, Faculty of Health and Medical Science, Adelaide 5000, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mary M","family":"Kavurma","sequence":"additional","affiliation":[{"name":"Heart Research Institute, Sydney 2042, Australia"},{"name":"The University of Sydney, Sydney Medical School, Sydney 2006, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0682-8760","authenticated-orcid":false,"given":"Christina A","family":"Bursill","sequence":"additional","affiliation":[{"name":"South Australian Health and Medical Research Institute, Vascular Research Centre, Adelaide 5000, Australia"},{"name":"University of Adelaide, Faculty of Health and Medical Science, Adelaide 5000, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2020,3,20]]},"reference":[{"key":"2021092910120613300_cvaa072-B1","doi-asserted-by":"crossref","first-page":"f6625","DOI":"10.1136\/bmj.f6625","article-title":"Bare metal stents, durable polymer drug eluting stents, and biodegradable polymer drug eluting stents for coronary artery disease: mixed treatment comparison meta-analysis","volume":"347","author":"Bangalore","year":"2013","journal-title":"BMJ"},{"key":"2021092910120613300_cvaa072-B2","doi-asserted-by":"crossref","first-page":"606","DOI":"10.1093\/eurheartj\/ehr479","article-title":"Lower risk of stent thrombosis and restenosis with unrestricted use of 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