Reverse Cholesterol Transport Dysfunction Is a Feature of Familial Hypercholesterolemia
Purpose of Review: We seek to establish whether high-density lipoprotein HDL metabolism and reverse cholesterol transport (RCT) impairment is an intrinsic feature of familial hypercholesterolemia (FH). Recent Findings: RCT from macrophages (m-RCT), a vascular cell type of major influence on atherosc...
| Autores: | , , , |
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| Tipo de recurso: | artículo |
| Fecha de publicación: | 2021 |
| País: | España |
| Institución: | Universitat Autònoma de Barcelona |
| Repositorio: | Dipòsit Digital de Documents de la UAB |
| Idioma: | inglés |
| OAI Identifier: | oai:ddd.uab.cat:273040 |
| Acceso en línea: | https://ddd.uab.cat/record/273040 https://dx.doi.org/urn:doi:10.1007/s11883-021-00928-1 |
| Access Level: | acceso abierto |
| Palabra clave: | HDL LDL receptor Macrophage Autosomal dominant hypercholesterolemia |
| Sumario: | Purpose of Review: We seek to establish whether high-density lipoprotein HDL metabolism and reverse cholesterol transport (RCT) impairment is an intrinsic feature of familial hypercholesterolemia (FH). Recent Findings: RCT from macrophages (m-RCT), a vascular cell type of major influence on atherosclerosis, is impaired in FH due to defective low-density lipoprotein receptor (LDLR) function via both the HDL- and LDL-mediated pathways. Potential mechanisms include impaired HDL metabolism, which is linked to increased LDL levels, as well as the increased transport of cellular unesterified cholesterol to LDL, which presents a defective catabolism. Summary: RCT dysfunction is consistently associated with mutation-positive FH linked to decreased HDL levels as well as impaired HDL remodeling and LDLR function. It remains to be explored whether these alterations are also present in less well-characterized forms of FH, such as cases with no identified mutations, and whether they are fully corrected by current standard treatments. |
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