High HDL-Cholesterol Paradox: SCARB1-LAG3-HDL Axis.

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Abstrakt

Tytuł:: High HDL-Cholesterol Paradox: SCARB1-LAG3-HDL Axis.
Autorzy:: Rodriguez A; Cell Biology, Linda and David Roth Chair of Cardiovascular Health, Center for Vascular Biology, University of Connecticut Health, 263 Farmington Avenue, Farmington, CT, 06030, USA. .
Źródło:: Current atherosclerosis reports [Curr Atheroscler Rep] 2021 Jan 05; Vol. 23 (1), pp. 5. Date of Electronic Publication: 2021 Jan 05.
Typ publikacji:: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
Język:: English
Imprint Name(s):: Publication: <2010- > : Dordrecht, Netherlands : Springer
Original Publication: Philadelphia, PA : Current Science, 1999-
MeSH Terms:: Antigens, CD/*metabolism
Atherosclerosis/*metabolism
Cholesterol, HDL/*metabolism
Scavenger Receptors, Class B/*metabolism
Antigens, CD/genetics ; Atherosclerosis/genetics ; Atherosclerosis/mortality ; Cholesterol, HDL/blood ; Cholesterol, HDL/genetics ; Gene Expression Regulation/physiology ; Humans ; Scavenger Receptors, Class B/genetics ; Lymphocyte Activation Gene 3 Protein
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Contributed Indexing:: Keywords: Genetics; HDL-cholesterol; Mortality; Myocardial infarction
Substance Nomenclature:: 0 (Antigens, CD)
0 (Cholesterol, HDL)
0 (SCARB1 protein, human)
0 (Scavenger Receptors, Class B)
0 (Lymphocyte Activation Gene 3 Protein)
0 (Lag3 protein, human)
Entry Date(s):: Date Created: 20210105 Date Completed: 20210726 Latest Revision: 20221207
Update Code:: 20240105
PubMed Central ID:: PMC7782461
DOI:: 10.1007/s11883-020-00902-3
PMID:: 33398433
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Purpose of the Review: To evaluate recent studies related to the paradox of high HDL-C with mortality and atherosclerotic cardiovascular disease (ASCVD) risk.
Recent Findings: Two observational studies (Cardiovascular Health in Ambulatory Care Research Team [CANHEART] and Copenhagen City Heart Study and the Copenhagen General Population Study [Copenhagen Heart Studies]) of adults without pre-existing ASCVD have shown a significant U-shaped association of HDL-C with all-cause and cause-specific mortality. Both studies showed that low HDL-C levels consistently increased hazard risk (HR) for all-cause and cause-specific mortality. In the CANHEART study, high HDL-C levels, HDL-C > 90 mg/dL, were associated with increased HR for non-CVD/non-cancer mortality. In the Copenhagen Heart Studies, women with HDL-C ≥ 135 mg/dL showed increased HR for all-cause and CVD mortality, while men with HDL-C > 97 mg/dL showed increased HR for all-cause and CVD mortality. Genetic association studies failed to show that genetic etiologies of high HDL-C significantly reduced risk for myocardial infarction (MI), while hepatocyte nuclear factor-4 (HNF4A) was significantly associated with high HDL-C and increased MI risk. Candidate gene studies have identified scavenger receptor B class I (SCARB1) and lymphocyte activation gene-3 (LAG3) as genes significantly associated with high HDL-C and increased MI risk. Low HDL-C remains as a significant factor for increased disease risk while high HDL-C levels are not associated with cardioprotection. Clinical CVD risk calculators need revision.

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