{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T15:11:29Z","timestamp":1788966689589,"version":"build-2803163510"},"reference-count":52,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","license":[{"start":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T00:00:00Z","timestamp":1788220800000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:sec>\n                    <jats:title>Background and purpose:<\/jats:title>\n                    <jats:p>Inhibition of proprotein convertase subtilisin\/kexin type 9 (PCSK9) has emerged as a key therapeutic target for lowering low-density lipoprotein cholesterol (LDL-C). This study aimed to evaluate the LDL-C-lowering efficacy of a PCSK9-targeting aptamer (AP-1) in a hypercholesterolemic rat model.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental approach:<\/jats:title>\n                    <jats:p>Wistar male rats (n = 48) were divided into 8 groups (n = 6): normal control, negative control, positive control receiving atorvastatin (4 mg\/kg body weight) plus ezetimibe (1 mg\/kg BW), and a PBS vehicle group. Experimental groups received the aptamer intraperitoneally at 1, 3, and 8 \u03bcM;, and one group received 3 \u03bcM; aptamer combined with atorvastatin (4 mg\/kg BW). Hypercholesterolemia was induced for over 90 days, followed by a 4-week treatment period. Serum lipid parameters, including triglycerides (TG), total cholesterol (T-Chol), LDL-C, and atherogenic indices, were assessed.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Findings\/Results:<\/jats:title>\n                    <jats:p>TG, 143.2 \u00b1 16.44 vs. 109 \u00b1 23.05 mg\/dL; T-Chol, 88 \u00b1 3.11 vs. 80 \u00b1 7.16 mg\/dL, and LDL-C, 19.4 \u00b1 1.12 vs. 14.5 \u00b1 1.56 mg\/dL, levels were significantly increased in the hypercholesterolemic rat model compared to the normal group. Treatment with the 3 \u03bcM; aptamer produced the most pronounced lipidlowering effects, significantly reducing TG, 95.2 \u00b1 8.76 vs. 143.2 \u00b1 16.44 mg\/dL; T-Chol, 61.2 \u00b1 5.11 vs. 88 \u00b1 3.11 mg\/dL, and LDL-C, 11.4 \u00b1 0.75 vs. 19.4 \u00b1 1.12 compared to the hypercholesterolemic control group. Furthermore, the atherogenic index of plasma, remnant cholesterol, and Castelli risk index-II were reduced significantly.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion and implications:<\/jats:title>\n                    <jats:p>AP-1 aptamer-mediated PCSK9 inhibition significantly improved lipid profiles and atherogenic indices, supporting aptamers as a viable alternative to monoclonal antibody-based PCSK9 inhibition.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.4103\/rps.rps_242_25","type":"journal-article","created":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T10:19:01Z","timestamp":1788949141000},"page":"670-681","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":0,"title":["Aptamer targeting proprotein convertase subtilisin\/kexin type 9: in vivo efficacy in a hypercholesterolemic rat model"],"prefix":"10.4103","volume":"21","author":[{"given":"Yaser Eshaghi","family":"Milasi","sequence":"first","affiliation":[{"name":"Department of Clinical Biochemistry, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fariba","family":"Sakhaei","sequence":"additional","affiliation":[{"name":"Department of Clinical Biochemistry, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"AbbasAli","family":"Palizban","sequence":"additional","affiliation":[{"name":"Department of Clinical Biochemistry, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2026,9,8]]},"reference":[{"issue":"32","key":"R1-20260909","doi-asserted-by":"crossref","first-page":"2459","DOI":"10.1093\/eurheartj\/ehx144","article-title":"Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. 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