Free Cholesterol Bioavailability and Atherosclerosis
Abstract
As both a cholesterol acceptor and carrier in the reverse cholesterol transport (RCT) pathway, high-density lipoprotein (HDL) is putatively atheroprotective. However, current pharmacological therapies to increase plasma HDL cholesterol (HDL-c) concentration have paradoxically failed to prevent or reduce atherosclerosis and cardiovascular disease (CVD). Given that free cholesterol (FC) transfer between surfaces of lipoproteins and cells is reversible, excess plasma FC can be transferred to the cells of peripheral tissue sites resulting in atherosclerosis. Here, we summarize potential mechanisms contributing to this paradox and highlight the role of excess free cholesterol (FC) bioavailability in atherosclerosis vs. atheroprotection.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Mar 25, 2022
- Source ID
- 10.1007/s11883-022-01011-z
Entities
People
- Abrar Mamun
- Elizabeth A. Olmsted-Davis
- Henry Pownall
- John P. Cooke
- Jun-ichi Abe
- Longhou Fang
- Minh T. H. Nguyen
- Nhat-tu Le
- Priyanka Banerjee
- Rei J. Abe
Organizations
- National Institutes of Health