NDLI: Monogenic causes of elevated HDL cholesterol and implications for development of new therapeutics

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Volume 13, 2018

Volume 12, 2017

Type 2 diabetes: ceramides as a therapeutic target?

Offspring from mothers versus fathers with familial hypercholesterolemia: is there a difference in cardiovascular risk?

Does liver-derived ANGPTL3 play a role in cardiometabolic risk? Current evidence and future perspectives

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Sideritis euboea extract lowers total cholesterol but not LDL cholesterol in humans: a randomized controlled trial

Monogenic causes of elevated HDL cholesterol and implications for development of new therapeutics

Investigating sitosterolemia to understand lipid physiology

Lipid signals and insulin resistance

Fenofibrate and renal disease: clinical effects in diabetes

Ceramide in cystic fibrosis

Lipoprotein apheresis: an update

Monogenic causes of elevated HDL cholesterol and implications for development of new therapeutics

Content Provider	Taylor & Francis Online
Author	Larach, Daniel B. Cuchel, Marina Rader, Daniel J.
Abstract	Identification of the CETP, LIPG (encoding endothelial lipase) and APOC3 genes, and analysis of rare genetic variants in them, have allowed researchers to increase understanding of HDL metabolism significantly. However, development of cardiovascular risk-reducing therapeutics targeting the proteins encoded by these genes has been less straightforward. The failure of two CETP inhibitors is complex but illustrates a possible over-reliance on HDL cholesterol as a marker of therapeutic efficacy. The case of endothelial lipase exemplifies the importance of utilizing population-wide genetic studies of rare variants in potential therapeutic targets to gain information on cardiovascular disease end points. Similar population-wide studies of cardiovascular end points make apoC-III a potentially attractive target for lipid-related drug discovery. These three cases illustrate the positives and negatives of single-gene studies relating to HDL-related cardiovascular drug discovery; such studies should focus not only on HDL cholesterol and other components of the lipid profile, but also on the effect genetic variants have on cardiovascular end points.
Starting Page	635
Ending Page	648
Page Count	14
File Format	PDF HTM / HTML
ISSN	17584299 17584302
Journal	Clinical Lipidology
Volume Number	8
Issue Number	6
DOI	10.2217/clp.13.73
Language	English
Publisher	Taylor & Francis
Publisher Date	2017-01-18
Access Restriction	Open
Subject Keyword	Anacetrapib ApoC-III CETP Cholesterol Dalcetrapib Endothelial lipase Evacetrapib Genetics HDL ISI-APOCIIIrx Torcetrapib
Content Type	Text
Subject	Endocrinology, Diabetes and Metabolism Cardiology and Cardiovascular Medicine

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Monogenic causes of elevated HDL cholesterol and implications for development of new therapeutics

Modulating cholesteryl ester transfer protein activity maintains efficient pre-β-HDL formation and increases reverse cholesterol transport.

CETP antagonism versus agonism in cardiovascular prevention and plaque regression

Therapeutic inhibition of apoC-III for the treatment of hypertriglyceridemia

Cholesteryl Ester Transfer Protein Inhibition in Cardiovascular Risk Management: Ongoing Trials will End the Confusion

Assessing the mechanisms of cholesteryl ester transfer protein inhibitors

Atorvastatin Decreases Apolipoprotein C-III in Apolipoprotein B-Containing Lipoprotein and HDL in Type 2 Diabetes: A potential mechanism to lower plasma triglycerides

Changing paradigm in HDL metabolism and cellular effects

Free cholesterol transfer to high-density lipoprotein (HDL) upon triglyceride lipolysis underlies the U-shape relationship between HDL-cholesterol and cardiovascular disease

Monogenic causes of elevated HDL cholesterol and implications for development of new therapeutics

Similar Documents

Monogenic causes of elevated HDL cholesterol and implications for development of new therapeutics

Modulating cholesteryl ester transfer protein activity maintains efficient pre-β-HDL formation and increases reverse cholesterol transport.

CETP antagonism versus agonism in cardiovascular prevention and plaque regression

Therapeutic inhibition of apoC-III for the treatment of hypertriglyceridemia

Cholesteryl Ester Transfer Protein Inhibition in Cardiovascular Risk Management: Ongoing Trials will End the Confusion

Assessing the mechanisms of cholesteryl ester transfer protein inhibitors

Atorvastatin Decreases Apolipoprotein C-III in Apolipoprotein B-Containing Lipoprotein and HDL in Type 2 Diabetes: A potential mechanism to lower plasma triglycerides

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Free cholesterol transfer to high-density lipoprotein (HDL) upon triglyceride lipolysis underlies the U-shape relationship between HDL-cholesterol and cardiovascular disease

Monogenic causes of elevated HDL cholesterol and implications for development of new therapeutics