{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T20:04:05Z","timestamp":1789502645150,"version":"build-2803163510"},"reference-count":54,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"9","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2023,2,28]]},"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>The metalloprotease ADAMTS-7 (a disintegrin and metalloproteinase with thrombospondin type 1 motif 7) is a novel locus associated with human coronary atherosclerosis. ADAMTS-7 deletion protects against atherosclerosis and vascular restenosis in rodents.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>\n                      We designed 3 potential vaccines consisting of distinct B cell epitopic peptides derived from ADAMTS-7 and conjugated with the carrier protein KLH (keyhole limpet hemocyanin) as well as aluminum hydroxide as an adjuvant. Arterial ligation or wire injury was used to induce neointima in mice, whereas\n                      <jats:italic>ApoE<\/jats:italic>\n                      <jats:sup>-\/-<\/jats:sup>\n                      and\n                      <jats:italic>LDLR<\/jats:italic>\n                      <jats:sup>-\/-<\/jats:sup>\n                      (LDLR [low-density lipoprotein receptor]) mice fed a high-fat diet were applied to assess atherosclerosis. In addition, coronary stent implantation was performed on vaccine-immunized Bama miniature pigs, followed by optical coherence tomography to evaluate coronary intimal hyperplasia.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      A vaccine, ATS7vac, was screened out from 3 candidates to effectively inhibit intimal thickening in murine carotid artery ligation models after vaccination. As well, immunization with ATS7vac alleviated neointima formation in murine wire injury models and mitigated atherosclerotic lesions in both hyperlipidemic\n                      <jats:italic>ApoE<\/jats:italic>\n                      <jats:sup>-\/-<\/jats:sup>\n                      and\n                      <jats:italic>LDLR<\/jats:italic>\n                      <jats:sup>-\/-<\/jats:sup>\n                      mice without lowering lipid levels. Preclinically, ATS7vac markedly impeded intimal hyperplasia in swine stented coronary arteries, but without significant immune-related organ injuries. Mechanistically, ATS7vac vaccination produced specific antibodies against ADAMTS-7, which markedly repressed ADAMTS-7\u2013mediated COMP (cartilage oligomeric matrix protein) and TSP-1 (thrombospondin-1) degradation and subsequently inhibited vascular smooth muscle cell migration but promoted re-endothelialization.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>ATS7vac is a novel atherosclerosis vaccine that also alleviates in-stent restenosis. The application of ATS7vac would be a complementary therapeutic avenue to the current lipid-lowering strategy for atherosclerotic disease.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/circulationaha.122.061516","type":"journal-article","created":{"date-parts":[[2022,12,23]],"date-time":"2022-12-23T05:00:31Z","timestamp":1671771631000},"page":"728-742","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":74,"title":["Peptide Vaccine Against ADAMTS-7 Ameliorates Atherosclerosis and Postinjury Neointima Hyperplasia"],"prefix":"10.1161","volume":"147","author":[{"given":"Zihan","family":"Ma","sequence":"first","affiliation":[{"name":"Department of Physiology and Pathophysiology (Z.M., C.M., S.Y., Y.J., R.G., F.Y., X.W., Y.F., W.K.), Peking University, Beijing, China."},{"name":"Key Laboratory of Molecular Cardiovascular Science (Z.M., C.M., S.Y., Y.J., R.G., F.Y., X.W., Y.F., W.K.), Ministry of Education, Beijing, 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