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Cited by 89

The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.

Update on Dyslipidemia

Garg, Abhimanyu, Simha, Vinaya·2007·The Journal of Clinical Endocrinology & Metabolism
DOI 10.1210/jc.2007-0275
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Abstract

Recently, considerable progress has been made in understanding the genetic basis of dyslipidemias and in studying the safety and efficacy of lipid-lowering drugs for coronary heart disease (CHD) prevention. Novel loci have been identified for monogenic hypercholesterolemia, such as low-density lipoprotein (LDL) receptor (LDLR)-associated protein, proprotein convertase subtilisin-like kexin type 9, and ATP-binding cassette transporters ABCG5 and ABCG8. LDLR-associated protein promotes clustering of LDLRs into clathrin-coated pits for LDL uptake; proprotein convertase subtilisin-like kexin type 9 is involved in LDLR degradation; and ABCG5 and 8 pump sterols out of the hepatic and intestinal cells into bile and intestinal lumen, respectively. A novel gene encoding apolipoprotein AV, an activator of lipoprotein lipase, has also been linked to familial hypertriglyceridemia. Linkage of familial combined hyperlipidemia to upstream stimulatory factor 1 remains controversial. Recent guidelines of the Adult Treatment Panel III emphasize intensive reduction of LDL or non-high-density lipoprotein cholesterol in patients at high risk of CHD. However, of the four recently concluded trials comparing high- vs. low-dose statin therapy, only two showed an unequivocal reduction in cardiovascular endpoints. Because intensive statin therapy can increase the risk of myopathy and hepatotoxicity, it is important to consider its risk-benefit ratio in individual patients. Restriction of dietary satura…

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Crossref · 10.1210/jc.2007-0275

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12 of 12 references verified0 citation errors · 0 not checkable

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  • Increasing the amount of LDLR protein in the liver could be a therapeutic approach for hyperlipidemia.

    “It has been reported that increasing the amount of LDLR protein in the liver could be a therapeutic approach for hyperlipidemia (28).”

    From ZFP36L1 and ZFP36L2 control LDLR mRNA stability via the ERK–RSK pathway (2014) · cites this paper as [28]

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Metadata

Authors
Garg, A., & Simha, V.
Venue
The Journal of Clinical Endocrinology & Metabolism
Publisher
The Endocrine Society
Published
2007-05
Volume
92
Issue
5
Pages
1581-1589
ISSN
  • 0021-972X
  • 1945-7197
DOI
10.1210/jc.2007-0275
Cited by
89
References
12
Language
en

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