ReviewCurrent atherosclerosis reports2021
Reverse Cholesterol Transport Dysfunction Is a Feature of Familial Hypercholesterolemia.
Review in Current atherosclerosis reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Integrative bioinformatics analysis identifies APOE as a candidate link between lipid dysregulation and macrophage activation in inborn errors of metabolism.Frontiers in pharmacology · 2026Article
- HDL cholesterol as an associate of prevalent coronary artery disease in heterozygous Familial hypercholesterolemia beyond LDL cholesterol.Endocrine · 2025Article
- Nuclear receptors in metabolic, inflammatory, and oncologic diseases: mechanisms, therapeutic advances, and future directions.European journal of medical research · 2025Review
- Quo Vadis after AEGIS: New Opportunities for Therapies Targeted at Reverse Cholesterol Transport?Current atherosclerosis reports · 2025Review
- PCSK9 Antibodies Treatment Specifically Enhances the Macrophage-specific Reverse Cholesterol Transport Pathway in Heterozygous Familial Hypercholesterolemia.JACC. Basic to translational science · 2024Article
- Review
- HDL Function and Atherosclerosis: Reactive Dicarbonyls as Promising Targets of Therapy.Circulation research · 2023Review
- Cholesterol efflux capacity is increased in subjects with familial hypercholesterolemia in a retrospective case-control study.Scientific reports · 2023Article
- Capacity of HDL to Efflux Cellular Cholesterol from Lipid-Loaded Macrophages Is Reduced in Patients with Familial Hypercholesterolemia.Metabolites · 2023Article
- HDL Cholesterol Efflux and Serum Cholesterol Loading Capacity Alterations Associate to Macrophage Cholesterol Accumulation in FH Patients with Achilles Tendon Xanthoma.International journal of molecular sciences · 2022Article
- High-Density Lipoprotein Changes in Alzheimer's Disease AreBiomedicines · 2022Article
- Whole-exome sequencing reveals damaging gene variants associated with hypoalphalipoproteinemia.Journal of lipid research · 2022Article
- Familial Hypercholesterolemia: Do HDL Play a Role?Biomedicines · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of reviewWe seek to establish whether high-density lipoprotein HDL metabolism and reverse cholesterol transport (RCT) impairment is an intrinsic feature of familial hypercholesterolemia (FH). RECENT
findingsRCT 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. 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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.