The Role of Antisense Therapies Targeting Lipoprotein(a)
Atherosclerotic cardiovascular disease (ASCVD) continues to be the leading cause of preventable death in the United States. Elevated low-density lipoprotein cholesterol (LDL-C) is well known to result in cardiovascular disease. Mainstay therapy for reducing LDL-C and ASCVD risk is statin therapy. De...
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| Veröffentlicht in: | Journal of cardiovascular pharmacology 2021-07, Vol.78 (1), p.e5-e11 |
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| container_title | Journal of cardiovascular pharmacology |
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| creator | Plakogiannis, Roda Sorbera, Maria Fischetti, Briann Chen, Mandy |
| description | Atherosclerotic cardiovascular disease (ASCVD) continues to be the leading cause of preventable death in the United States. Elevated low-density lipoprotein cholesterol (LDL-C) is well known to result in cardiovascular disease. Mainstay therapy for reducing LDL-C and ASCVD risk is statin therapy. Despite achieving desired LDL-C levels with lipid-lowering therapy, cardiovascular residual risk often persists. Elevated lipoprotein(a) [Lp(a)] levels have been highlighted as an inherent independent predictor of ASCVD, and decreasing Lp(a) levels may result in a significant reduction in the residual risk in high-risk patients. To date, there are no approved medications to lower Lp(a) levels. Nicotinic acid, proprotein convertase subtilisin/kexin 9 inhibitors, and antisense oligonucleotide have demonstrated modest to potent Lp(a) reduction. Spotlight has been placed on antisense oligonucleotides and their role in Lp(a) lowering. APO(a)LRx is in the frontline for selectively decreasing Lp(a) concentrations and ongoing research may prove that this medication may lower Lp(a)-mediated residual risk, translating into cardiovascular benefit. |
| doi_str_mv | 10.1097/FJC.0000000000001045 |
| format | Article |
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Elevated low-density lipoprotein cholesterol (LDL-C) is well known to result in cardiovascular disease. Mainstay therapy for reducing LDL-C and ASCVD risk is statin therapy. Despite achieving desired LDL-C levels with lipid-lowering therapy, cardiovascular residual risk often persists. Elevated lipoprotein(a) [Lp(a)] levels have been highlighted as an inherent independent predictor of ASCVD, and decreasing Lp(a) levels may result in a significant reduction in the residual risk in high-risk patients. To date, there are no approved medications to lower Lp(a) levels. Nicotinic acid, proprotein convertase subtilisin/kexin 9 inhibitors, and antisense oligonucleotide have demonstrated modest to potent Lp(a) reduction. Spotlight has been placed on antisense oligonucleotides and their role in Lp(a) lowering. APO(a)LRx is in the frontline for selectively decreasing Lp(a) concentrations and ongoing research may prove that this medication may lower Lp(a)-mediated residual risk, translating into cardiovascular benefit.</description><identifier>ISSN: 0160-2446</identifier><identifier>EISSN: 1533-4023</identifier><identifier>DOI: 10.1097/FJC.0000000000001045</identifier><identifier>PMID: 34232223</identifier><language>eng</language><publisher>United States: Journal of Cardiovascular Pharmacology</publisher><subject>Atherosclerosis - blood ; Atherosclerosis - drug therapy ; Atherosclerosis - genetics ; Biomarkers - blood ; Clinical Trials as Topic ; Down-Regulation ; Dyslipidemias - blood ; Dyslipidemias - drug therapy ; Dyslipidemias - genetics ; Evidence-Based Medicine ; Humans ; Hypolipidemic Agents - adverse effects ; Hypolipidemic Agents - therapeutic use ; Lipoprotein(a) - blood ; Oligodeoxyribonucleotides, Antisense - adverse effects ; Oligodeoxyribonucleotides, Antisense - therapeutic use ; Oligonucleotides - adverse effects ; Oligonucleotides - therapeutic use ; Treatment Outcome</subject><ispartof>Journal of cardiovascular pharmacology, 2021-07, Vol.78 (1), p.e5-e11</ispartof><rights>Journal of Cardiovascular Pharmacology</rights><rights>Copyright © 2021 Wolters Kluwer Health, Inc. 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Elevated low-density lipoprotein cholesterol (LDL-C) is well known to result in cardiovascular disease. Mainstay therapy for reducing LDL-C and ASCVD risk is statin therapy. Despite achieving desired LDL-C levels with lipid-lowering therapy, cardiovascular residual risk often persists. Elevated lipoprotein(a) [Lp(a)] levels have been highlighted as an inherent independent predictor of ASCVD, and decreasing Lp(a) levels may result in a significant reduction in the residual risk in high-risk patients. To date, there are no approved medications to lower Lp(a) levels. Nicotinic acid, proprotein convertase subtilisin/kexin 9 inhibitors, and antisense oligonucleotide have demonstrated modest to potent Lp(a) reduction. Spotlight has been placed on antisense oligonucleotides and their role in Lp(a) lowering. APO(a)LRx is in the frontline for selectively decreasing Lp(a) concentrations and ongoing research may prove that this medication may lower Lp(a)-mediated residual risk, translating into cardiovascular benefit.</description><subject>Atherosclerosis - blood</subject><subject>Atherosclerosis - drug therapy</subject><subject>Atherosclerosis - genetics</subject><subject>Biomarkers - blood</subject><subject>Clinical Trials as Topic</subject><subject>Down-Regulation</subject><subject>Dyslipidemias - blood</subject><subject>Dyslipidemias - drug therapy</subject><subject>Dyslipidemias - genetics</subject><subject>Evidence-Based Medicine</subject><subject>Humans</subject><subject>Hypolipidemic Agents - adverse effects</subject><subject>Hypolipidemic Agents - therapeutic use</subject><subject>Lipoprotein(a) - blood</subject><subject>Oligodeoxyribonucleotides, Antisense - adverse effects</subject><subject>Oligodeoxyribonucleotides, Antisense - therapeutic use</subject><subject>Oligonucleotides - adverse effects</subject><subject>Oligonucleotides - therapeutic use</subject><subject>Treatment Outcome</subject><issn>0160-2446</issn><issn>1533-4023</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkFtLw0AQhRdRbK3-A5E81ofU2d3ZTfJYivVCQZD6HLbbSRtNk7ibUPz3prZecF6GOZw5Bz7GLjmMOCTRzfRxMoI_wwHVEetzJWWIIOQx6wPXEApE3WNn3r92HlSRPmU9iUIKIWSfxfM1Bc9VQUGVBeOyyT2VnoJOdabOyQdz41bU5OUqmOV1VbuqobwcmutzdpKZwtPFYQ_Yy_R2PrkPZ093D5PxLLTIYxkKLciijBXCUvHESgSlM0ORBki0tVYszFKgMtYYlcQxmTiDyCxkQppniHLAhvvcrvq9Jd-km9xbKgpTUtX6VChMBGCEvLPi3mpd5b2jLK1dvjHuI-WQ7pilHbP0P7Pu7erQ0C42tPx5-ob0m7utioacfyvaLbl0TaZo1l95SiKGAgSHqLvCnSTlJ6cYdE0</recordid><startdate>20210701</startdate><enddate>20210701</enddate><creator>Plakogiannis, Roda</creator><creator>Sorbera, Maria</creator><creator>Fischetti, Briann</creator><creator>Chen, Mandy</creator><general>Journal of Cardiovascular Pharmacology</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20210701</creationdate><title>The Role of Antisense Therapies Targeting Lipoprotein(a)</title><author>Plakogiannis, Roda ; Sorbera, Maria ; Fischetti, Briann ; Chen, Mandy</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4183-262ec438540d519c34056fae760096ccc2bad245acaa5988ea8f07ab39e61f443</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Atherosclerosis - blood</topic><topic>Atherosclerosis - drug therapy</topic><topic>Atherosclerosis - genetics</topic><topic>Biomarkers - blood</topic><topic>Clinical Trials as Topic</topic><topic>Down-Regulation</topic><topic>Dyslipidemias - blood</topic><topic>Dyslipidemias - drug therapy</topic><topic>Dyslipidemias - genetics</topic><topic>Evidence-Based Medicine</topic><topic>Humans</topic><topic>Hypolipidemic Agents - adverse effects</topic><topic>Hypolipidemic Agents - therapeutic use</topic><topic>Lipoprotein(a) - blood</topic><topic>Oligodeoxyribonucleotides, Antisense - adverse effects</topic><topic>Oligodeoxyribonucleotides, Antisense - therapeutic use</topic><topic>Oligonucleotides - adverse effects</topic><topic>Oligonucleotides - therapeutic use</topic><topic>Treatment Outcome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Plakogiannis, Roda</creatorcontrib><creatorcontrib>Sorbera, Maria</creatorcontrib><creatorcontrib>Fischetti, Briann</creatorcontrib><creatorcontrib>Chen, Mandy</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cardiovascular pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Plakogiannis, Roda</au><au>Sorbera, Maria</au><au>Fischetti, Briann</au><au>Chen, Mandy</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Role of Antisense Therapies Targeting Lipoprotein(a)</atitle><jtitle>Journal of cardiovascular pharmacology</jtitle><addtitle>J Cardiovasc Pharmacol</addtitle><date>2021-07-01</date><risdate>2021</risdate><volume>78</volume><issue>1</issue><spage>e5</spage><epage>e11</epage><pages>e5-e11</pages><issn>0160-2446</issn><eissn>1533-4023</eissn><abstract>Atherosclerotic cardiovascular disease (ASCVD) continues to be the leading cause of preventable death in the United States. Elevated low-density lipoprotein cholesterol (LDL-C) is well known to result in cardiovascular disease. Mainstay therapy for reducing LDL-C and ASCVD risk is statin therapy. Despite achieving desired LDL-C levels with lipid-lowering therapy, cardiovascular residual risk often persists. Elevated lipoprotein(a) [Lp(a)] levels have been highlighted as an inherent independent predictor of ASCVD, and decreasing Lp(a) levels may result in a significant reduction in the residual risk in high-risk patients. To date, there are no approved medications to lower Lp(a) levels. Nicotinic acid, proprotein convertase subtilisin/kexin 9 inhibitors, and antisense oligonucleotide have demonstrated modest to potent Lp(a) reduction. Spotlight has been placed on antisense oligonucleotides and their role in Lp(a) lowering. APO(a)LRx is in the frontline for selectively decreasing Lp(a) concentrations and ongoing research may prove that this medication may lower Lp(a)-mediated residual risk, translating into cardiovascular benefit.</abstract><cop>United States</cop><pub>Journal of Cardiovascular Pharmacology</pub><pmid>34232223</pmid><doi>10.1097/FJC.0000000000001045</doi></addata></record> |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals |
| subjects | Atherosclerosis - blood Atherosclerosis - drug therapy Atherosclerosis - genetics Biomarkers - blood Clinical Trials as Topic Down-Regulation Dyslipidemias - blood Dyslipidemias - drug therapy Dyslipidemias - genetics Evidence-Based Medicine Humans Hypolipidemic Agents - adverse effects Hypolipidemic Agents - therapeutic use Lipoprotein(a) - blood Oligodeoxyribonucleotides, Antisense - adverse effects Oligodeoxyribonucleotides, Antisense - therapeutic use Oligonucleotides - adverse effects Oligonucleotides - therapeutic use Treatment Outcome |
| title | The Role of Antisense Therapies Targeting Lipoprotein(a) |
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