Medical College of Wisconsin
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Rediscovering scavenger receptor type BI: surprising new roles for the HDL receptor. Curr Opin Lipidol 2017 Jun;28(3):255-260

Date

03/17/2017

Pubmed ID

28301373

Pubmed Central ID

PMC5523812

DOI

10.1097/MOL.0000000000000413

Scopus ID

2-s2.0-85015644706 (requires institutional sign-in at Scopus site)   22 Citations

Abstract

PURPOSE OF REVIEW: Scavenger receptor BI (SR-BI) is classically known for its role in antiatherogenic reverse cholesterol transport as it selectively takes up cholesterol esters from HDL. Here, we have highlighted recent literature that describes novel functions for SR-BI in physiology and disease.

RECENT FINDINGS: A large population-based study has revealed that patients heterozygous for the P376L mutant form of SR-BI showed significantly increased levels of plasma HDL-cholesterol and had increased risk of cardiovascular disease, demonstrating that SR-BI in humans is a significant determinant of cardiovascular disease. Furthermore, SR-BI has been shown to modulate the susceptibility to LPS-induced tissue injury and the ability of sphingosine 1 phosphate to interact with its receptor, linking SR-BI to the regulation of inflammation. In addition, important domains within the molecule (Trp-415) as well as novel regulators (procollagen C-endopeptidase enhancer protein 2) of SR-BI's selective uptake function have recently been identified. Moreover, relatively high expression levels of the SR-BI protein have been observed in a variety of cancer tissues, which is associated with a reduced overall survival rate.

SUMMARY: The HDL receptor SR-BI is a potential therapeutic target not only in the cardiovascular disease setting, but also in inflammatory conditions as well as in cancer.

Author List

Hoekstra M, Sorci-Thomas M

Author

Mary Sorci Thomas PhD Professor in the Medicine department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Animals
Biomarkers, Tumor
CD36 Antigens
Humans
Inflammation
Molecular Targeted Therapy
Neoplasms