期刊
CIRCULATION RESEARCH
卷 124, 期 3, 页码 386-404出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/CIRCRESAHA.118.313171
关键词
atherosclerosis; dyslipidemias; humans; lipoprotein(a); oligonucleotides, antisense
资金
- Jacob J. Wolfe Distinguished Medical Research Chair
- Edith Schulich Vinet Research Chair in Human Genetics
- Martha G. Blackburn Chair in Cardiovascular Research
- Canadian Institutes of Health Research
- Heart and Stroke Foundation of Ontario [HSF-G-18-0022147]
- Fondation Leducq
- National Institutes of Health [P01-HL088093, P01-HL055798, R01-HL106579, R01-HL078610, R01-HL124174]
Several new or emerging drugs for dyslipidemia owe their existence, in part, to human genetic evidence, such as observations in families with rare genetic disorders or in Mendelian randomization studies. Much effort has been directed to agents that reduce LDL (low-density lipoprotein) cholesterol, triglyceride, and Lp[a] (lipoprotein[a]), with some sustained programs on agents to raise HDL (high-density lipoprotein) cholesterol. Lomitapide, mipomersen, AAV8.TBG.hLDLR, inclisiran, bempedoic acid, and gemcabene primarily target LDL cholesterol. Alipogene tiparvovec, pradigastat, and volanesorsen primarily target elevated triglycerides, whereas evinacumab and IONIS-ANGPTL3-L-Rx target both LDL cholesterol and triglyceride. IONIS-APO(a)-L-Rx targets Lp(a).
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