GO:0010983 positive regulation of high-density lipoprotein particle clearance: Reverse Cholesterol Transport Pathway, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0010983 describes any process that increases the rate or extent of high-density lipoprotein (HDL) particle clearance from the circulation [1,2].
• HDL clearance is primarily mediated by hepatic receptors such as SR-BI (SCARB1) and involves endocytic trafficking through clathrin-coated pits and endosomal compartments [1,8].
• Apolipoprotein A-I (APOA1) charge and conformation are critical determinants of HDL clearance rate in vivo.
• Dysregulation of HDL clearance contributes to dyslipidemia, atherosclerosis, and metabolic disorders, and is modulated by factors such as alcohol consumption and obstructive sleep apnea [4,5].
• Experimental models for studying this process include hepatocyte cell lines (HepG2), knockout mice, and CRISPR-engineered cell models targeting SCARB1, APOA1, and LRP1 [1,7,8].
• EDITGENE provides CRISPR knockout, point mutation, knock-in, overexpression, and library screening services to dissect the genetic regulation of HDL clearance.
Description
High-density lipoprotein (HDL) particles are central to reverse cholesterol transport, the process by which excess cholesterol is removed from peripheral tissues and delivered to the liver for excretion. The clearance of HDL particles from the circulation is a tightly regulated biological process, and its positive regulation—GO:0010983—encompasses the molecular events that accelerate this removal [1,2]. Understanding how HDL clearance is upregulated is critical for deciphering lipid metabolism and for developing therapeutic strategies against cardiovascular disease [4,8]. GO:0010983 is a biological process term that specifically refers to any mechanism that increases the frequency, rate, or extent of high-density lipoprotein particle clearance [1,2]. This process involves the recognition of HDL particles by cell surface receptors, internalization into endocytic compartments, and subsequent intracellular trafficking and degradation or recycling [1,7]. The term is distinct from general HDL metabolism because it focuses on the positive regulation of the clearance step, which can be modulated by apolipoprotein composition, receptor availability, and extracellular factors [2,5]. Researchers study GO:0010983 to identify genetic and pharmacological targets that enhance HDL clearance, which may have implications for conditions ranging from atherosclerosis to graft-versus-host disease [3,8]. The process is also relevant to understanding how lifestyle factors such as alcohol intake and sleep apnea influence lipid profiles [4,5]. By leveraging CRISPR-based gene editing, scientists can now precisely manipulate genes involved in this pathway to establish causal relationships and develop new therapeutic interventions [1,7].
positive regulation of high-density lipoprotein particle clearance At A Glance
| GO ID | GO:0010983 |
|---|---|
| GO term | positive regulation of high-density lipoprotein particle clearance |
| Ontology | biological_process |
| Synonym | None listed in QuickGO |
| Major function | Upregulation of the removal of HDL particles from circulation, primarily via hepatic receptors and endocytic pathways [1,8] |
| Related cellular component | Endocytic compartments (clathrin-coated pits, endosomes, lysosomes) |
| Key molecular players | APOA1, SCARB1 (SR-BI), LRP1, APOE [2,7,8] |
| Physiological context | Reverse cholesterol transport, lipid homeostasis |
| Disease relevance | Atherosclerosis, dyslipidemia, metabolic syndrome [4,8] |
What Is GO:0010983?
GO:0010983, positive regulation of high-density lipoprotein particle clearance, is a biological process that encompasses any molecular event or signaling pathway that increases the rate or extent of HDL particle removal from the bloodstream [1,2]. This includes enhanced receptor-mediated endocytosis, increased intracellular trafficking to lysosomes, and accelerated catabolism of HDL components [1,7]. The term is defined within the Gene Ontology as a positive regulatory process that acts on the clearance of HDL particles, which are spherical complexes of lipids and proteins (mainly APOA1) that mediate reverse cholesterol transport.
Why Is positive regulation of high-density lipoprotein particle clearance Important in Cell Biology?
GO:0010983 is important because HDL clearance directly influences plasma HDL cholesterol levels, which are inversely associated with cardiovascular disease risk. Positive regulation of this process can lower HDL levels, but it may also enhance reverse cholesterol transport if the cleared HDL is efficiently delivered to the liver for excretion. Dysregulation of HDL clearance is linked to dyslipidemia in conditions such as obstructive sleep apnea and chronic alcohol consumption [4,5]. Moreover, modulating HDL clearance has therapeutic potential in transplantation, as HDL infusion protects against graft-versus-host disease in experimental models. Thus, understanding the positive regulation of HDL clearance is essential for developing targeted therapies for metabolic and inflammatory diseases.
• Regulates plasma HDL cholesterol levels, a key biomarker for cardiovascular risk.
• Influences reverse cholesterol transport efficiency and overall cholesterol homeostasis.
• Implicated in dyslipidemia associated with obstructive sleep apnea.
• Modulated by ethanol consumption, which accelerates VLDL turnover and upregulates HDL.
• Genetic variants affecting HDL clearance are linked to obesity and serum lipid levels.
• Provides a therapeutic target for acute graft-versus-host disease, where HDL infusion is protective.
• Involves apolipoprotein A-I conformation and charge, which determine clearance rate.
• Requires endocytic trafficking machinery, including LRP1 and SR-BI, which are potential drug targets [1,7,8].
• Can be studied using CRISPR-engineered hepatocyte models to dissect causal genes [1,7].
• Relevant to personalized medicine approaches for lipid disorders.
What Happens During positive regulation of high-density lipoprotein particle clearance?
Recognition and Binding of HDL Particles to Cell Surface Receptors
In simple terms: HDL particles are recognized by specific receptors on liver cells, which grab them for removal.
The first step in positive regulation of HDL clearance is the recognition of HDL particles by cell surface receptors, primarily scavenger receptor class B type I (SR-BI, gene SCARB1) and the low-density lipoprotein receptor-related protein 1 (LRP1) [1,7,8]. SR-BI mediates selective cholesterol ester uptake from HDL without internalizing the entire particle, while LRP1 can bind apolipoprotein E (APOE) associated with HDL and facilitate endocytosis [7,8]. The charge and conformation of apolipoprotein A-I (APOA1) on the HDL surface regulate this binding step; reconstituted HDL with altered APOA1 charge shows different clearance rates in vivo. Positive regulation can occur through increased receptor expression or enhanced ligand affinity [2,8].
Endocytic Internalization and Trafficking to Endosomal Compartments
In simple terms: Once bound, HDL particles are taken into the cell and moved through a series of compartments for processing.
After receptor binding, HDL particles are internalized via clathrin-coated pits and delivered to early endosomes. In HepG2 cells, holo-HDL particle uptake leads to accumulation in endocytic compartments that can be distinguished by markers such as EEA1 and Rab5. LRP1 mediates endosomal trapping and recycling of APOE, which can influence the fate of HDL particles. Positive regulation of clearance may involve accelerated endosomal sorting to lysosomes for degradation or enhanced recycling of receptors back to the cell surface [1,7]. The endocytic pathway is a key checkpoint where regulatory signals can increase the rate of HDL processing.
Intracellular Degradation and Cholesterol Release
In simple terms: Inside the cell, HDL particles are broken down, and their cholesterol is released for excretion or reuse.
Following internalization, HDL particles are delivered to late endosomes and lysosomes where apolipoproteins and lipids are degraded. This step releases free cholesterol, which can be either excreted into bile or re-esterified for storage. Positive regulation of HDL clearance can enhance the delivery of HDL-derived cholesterol to the liver for biliary excretion, thereby promoting reverse cholesterol transport. In macrophages, SR-BI drives reverse cholesterol transport by facilitating cholesterol efflux to HDL, but in hepatocytes, SR-BI mediates the selective uptake of HDL cholesterol. The balance between degradation and recycling determines the net clearance rate [1,7].
Regulation by Apolipoprotein Composition and Extracellular Factors
In simple terms: The composition of HDL particles and external factors like alcohol can speed up or slow down their clearance.
The clearance of HDL particles is influenced by the apolipoprotein composition, particularly APOA1 charge and conformation. Reconstituted HDL with modified APOA1 shows altered clearance kinetics in vivo, indicating that positive regulation can be achieved by changing the particle's surface properties. Extracellular factors such as ethanol consumption accelerate VLDL triglyceride turnover and upregulate HDL, potentially by increasing clearance of triglyceride-rich lipoproteins. Obstructive sleep apnea is associated with dyslipidemia, including altered HDL levels, suggesting that intermittent hypoxia may affect HDL clearance pathways. Genetic factors also play a role, as bivariate genetic analysis has linked obesity-related genes to serum lipid levels.
Receptor Recycling and Cellular Homeostasis
In simple terms: After delivering their cargo, receptors can be recycled back to the cell surface to continue clearing more HDL.
Positive regulation of HDL clearance also involves the efficient recycling of receptors such as LRP1 and SR-BI back to the plasma membrane [7,8]. LRP1 undergoes endosomal trapping and recycling, which is dependent on its cytoplasmic tail and associated proteins. This recycling ensures sustained clearance capacity. In hepatocytes, SR-BI levels are regulated by transcriptional and post-transcriptional mechanisms, and its recycling is essential for continuous selective cholesterol uptake. Disruption of recycling leads to receptor degradation and reduced clearance, highlighting the importance of this step in the positive regulation of HDL clearance [7,8].
Key Genes Involved in GO:0010983 positive regulation of high-density lipoprotein particle clearance
The following genes and proteins are experimentally implicated in the positive regulation of high-density lipoprotein particle clearance, based on receptor binding, endocytic trafficking, and apolipoprotein composition studies.
| Gene | Major Role | Research Relevance |
|---|---|---|
| APOA1 | Major apolipoprotein of HDL; its charge and conformation regulate clearance | Target for modifying HDL clearance rate in vivo |
| SCARB1 (SR-BI) | Mediates selective cholesterol ester uptake from HDL in liver and steroidogenic tissues | Key receptor for reverse cholesterol transport and HDL clearance |
| LRP1 | Binds APOE on HDL and mediates endosomal trafficking and recycling | Regulates endosomal trapping and clearance of APOE-containing lipoproteins |
| APOE | Apolipoprotein that associates with HDL and facilitates receptor binding | Its recycling via LRP1 affects HDL clearance |
| ABCA1 | Mediates cholesterol efflux to lipid-poor APOA1, forming nascent HDL | Indirectly influences HDL clearance by determining HDL particle composition |
| ABCG1 | Promotes cholesterol efflux to mature HDL | Modulates HDL levels and reverse cholesterol transport |
| CETP | Transfers cholesteryl esters between HDL and apoB-containing lipoproteins | Affects HDL particle size and clearance |
| LCAT | Esterifies cholesterol on HDL, maintaining particle maturity | Influences HDL remodeling and clearance |
| PLTP | Phospholipid transfer protein; remodels HDL particles | Alters HDL size and receptor affinity |
| SR-BI (SCARB1) variants | Genetic polymorphisms affect HDL cholesterol levels | Link to obesity and serum lipid traits |
| LPL | Lipoprotein lipase; hydrolyzes triglycerides, affecting HDL metabolism | Ethanol-induced changes in LPL activity correlate with HDL upregulation |
| HL (LIPC) | Hepatic lipase; hydrolyzes HDL phospholipids and triglycerides | Modulates HDL clearance and size |
| EL (LIPG) | Endothelial lipase; phospholipase that reduces HDL levels | Potential target for increasing HDL |
| PON1 | Paraoxonase 1; associated with HDL, protects against oxidation | Influences HDL function and clearance |
| SAA | Serum amyloid A; acute-phase protein that displaces APOA1 on HDL | Inflammatory remodeling of HDL affects clearance |
| C1Q | Complement protein that binds HDL and may affect clearance | Role in inflammation and HDL metabolism |
| HIF-1α | Hypoxia-inducible factor; upregulated in sleep apnea, may affect lipid metabolism | Links intermittent hypoxia to dyslipidemia |
| ADIPOQ | Adiponectin; regulates lipid metabolism and insulin sensitivity | Genetic association with obesity and lipid levels |
How Is positive regulation of high-density lipoprotein particle clearance Regulated?
The positive regulation of HDL particle clearance is controlled at multiple levels, including receptor expression, apolipoprotein composition, and extracellular signals [1,2,8]. Transcriptional regulation of SCARB1 and LRP1 can increase receptor availability, enhancing clearance capacity [7,8]. Post-translational modifications of APOA1, such as oxidation or glycation, alter its charge and conformation, affecting receptor binding and clearance rate. Hormonal and metabolic factors, such as ethanol consumption, can upregulate HDL clearance by accelerating VLDL turnover and altering lipoprotein lipase activity. Inflammatory cytokines may also modulate HDL clearance by remodeling HDL particles through serum amyloid A displacement of APOA1. Additionally, hypoxia associated with obstructive sleep apnea may induce HIF-1α, which can affect lipid metabolism genes and potentially HDL clearance. Genetic variants in genes like SCARB1 and ADIPOQ have been linked to serum lipid levels and obesity, suggesting inherited differences in clearance regulation.
positive regulation of high-density lipoprotein particle clearance and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| SCARB1 | Atherosclerosis, dyslipidemia | Scarb1 knockout mouse; HepG2 SCARB1 KO cells |
| APOA1 | Cardiovascular disease, amyloidosis | Apoa1 knockout mouse; APOA1 mutant knock-in |
| LRP1 | Neurodegeneration, Alzheimer's disease | LRP1 conditional knockout mouse; iPSC-derived neurons |
| APOE | Alzheimer's disease, hyperlipidemia | APOE4 knock-in mouse; APOE KO HepG2 cells |
| SAA | Inflammation, graft-versus-host disease | SAA overexpression in mouse models of GVHD |
Atherosclerosis and Cardiovascular Disease
Dysregulation of HDL clearance is directly linked to atherosclerosis, as inefficient reverse cholesterol transport leads to cholesterol accumulation in arterial walls. Positive regulation of HDL clearance, when coupled with efficient biliary excretion, can be protective by enhancing reverse cholesterol transport. However, excessive clearance that lowers plasma HDL cholesterol may reduce the pool available for cholesterol efflux from macrophages, potentially exacerbating atherosclerosis. Genetic variations in SCARB1 and other HDL clearance genes are associated with altered cardiovascular risk [6,8]. Therapeutic strategies aimed at modulating HDL clearance must balance these opposing effects.
Metabolic Syndrome and Dyslipidemia
Metabolic syndrome is characterized by dyslipidemia, including low HDL cholesterol and high triglycerides [4,5]. Obstructive sleep apnea, a common comorbidity of metabolic syndrome, is associated with dyslipidemia, and intermittent hypoxia may alter HDL clearance pathways. Chronic alcohol consumption accelerates VLDL triglyceride turnover and upregulates HDL, possibly by increasing clearance of triglyceride-rich lipoproteins. Genetic studies have identified shared genetic architecture between obesity and serum lipid levels, implicating genes involved in HDL clearance. Thus, positive regulation of HDL clearance is a key node in metabolic dyslipidemia [4,5,6].
Graft-versus-Host Disease and Inflammation
HDL infusion protects against acute graft-versus-host disease in experimental allogeneic hematopoietic cell transplantation, suggesting that HDL particles and their clearance play a role in immune regulation. Inflammatory conditions can remodel HDL via serum amyloid A, which may affect clearance and function. Positive regulation of HDL clearance could therefore influence inflammatory diseases by altering the availability of functional HDL. Targeting HDL clearance pathways may offer therapeutic benefits in transplantation and inflammatory disorders.
Neurodegeneration and APOE Metabolism
APOE is a major genetic risk factor for Alzheimer's disease, and its metabolism is closely tied to HDL-like particles in the brain. LRP1 mediates endosomal trapping and recycling of APOE, which is relevant to HDL clearance pathways in the liver and possibly in the brain. Dysregulation of APOE clearance has been implicated in neurodegeneration, and positive regulation of HDL particle clearance may influence APOE levels and aggregation. Further research is needed to link GO:0010983 directly to neurodegenerative diseases.
From positive regulation of high-density lipoprotein particle clearance-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does SCARB1 mediate HDL clearance in hepatocytes? | SCARB1 knockout HepG2 cells generated by CRISPR [1,8] |
| How does APOA1 charge affect HDL clearance? | APOA1 point mutant knock-in mice or reconstituted HDL |
| What is the role of LRP1 in APOE recycling? | LRP1 knockout or tagged knock-in cell lines |
| Can overexpression of SR-BI increase HDL clearance? | SCARB1 overexpression in hepatocyte cell lines |
| Which genes regulate HDL clearance in response to ethanol? | Liver-specific CRISPR library screening in mouse models |
| Does HDL infusion protect against GVHD via clearance pathways? | Humanized mouse models of allogeneic transplantation |
How to Study the positive regulation of high-density lipoprotein particle clearance Process
| Method | What It Measures | Typical Application |
|---|---|---|
| CRISPR knockout screen | Genes required for HDL clearance | Identify positive regulators in HepG2 cells |
| Fluorescent HDL uptake assay | Binding and internalization rates | Compare control vs. mutant cells |
| Radiolabeled HDL clearance in vivo | Plasma clearance kinetics | Assess APOA1 charge effects in mice |
| Confocal microscopy | Co-localization with endosomal markers | Track HDL trafficking |
| Bivariate genetic analysis | Shared genetic architecture with lipid traits | Link obesity genes to HDL levels |
| Western blot | Receptor protein levels | Measure SCARB1 or LRP1 expression [7,8] |
| qPCR | mRNA expression of clearance genes | Validate knockout or overexpression |
| Flow cytometry | Cell surface receptor abundance | Quantify SR-BI recycling |
CRISPR Knockout Screening for HDL Clearance Regulators
Genome-wide CRISPR knockout screens can identify genes whose loss alters HDL particle clearance in hepatocyte cell lines [1,8]. Cells are transduced with a lentiviral sgRNA library, selected, and then incubated with fluorescently labeled HDL. Flow cytometry or imaging-based sorting enriches for cells with altered uptake, and sgRNA sequencing reveals candidate genes. This approach has been used to uncover endocytic trafficking genes required for holo-HDL uptake in HepG2 cells. Positive regulators are identified as those whose knockout reduces HDL clearance.
Biochemical Assays for HDL Binding and Internalization
Radiolabeled or fluorescent HDL particles are used to measure binding, internalization, and degradation in cultured cells [1,2]. For example, 125I-labeled HDL can assess clearance kinetics in vivo after injection into mice. In vitro, cell surface binding assays at 4°C distinguish binding from internalization, while chase experiments at 37°C measure endocytic trafficking. These methods quantify the positive regulation of HDL clearance by comparing control and genetically modified cells [1,2].
Imaging of Endocytic Compartments
Confocal microscopy and immunofluorescence can visualize the co-localization of HDL particles with endocytic markers such as EEA1, Rab5, and LAMP1. HepG2 cells incubated with fluorescent HDL show trafficking through early endosomes to lysosomes. Live-cell imaging allows real-time tracking of HDL uptake and recycling. These techniques reveal whether positive regulation involves accelerated endosomal sorting or enhanced lysosomal degradation.
Genetic Association and Bivariate Analysis
Bivariate genetic methods can explore the shared genetic architecture between obesity and serum lipid levels, including HDL cholesterol. Genome-wide association studies identify variants in genes such as SCARB1 and ADIPOQ that may affect HDL clearance. Mendelian randomization can test causality between gene expression and HDL levels. These approaches complement functional studies by highlighting pathways that regulate HDL clearance in human populations.
How CRISPR Can Be Used to Study GO:0010983 positive regulation of high-density lipoprotein particle clearance
Knockout
CRISPR knockout of candidate genes such as SCARB1, LRP1, or APOA1 in hepatocyte cell lines (e.g., HepG2) can determine their necessity for HDL clearance [1,7,8]. Knockout cells are generated using Cas9 and sgRNAs targeting early exons, followed by clonal selection and validation by sequencing and western blot. These models reveal whether a gene is a positive regulator by measuring reduced HDL uptake or clearance. For example, SCARB1 knockout abolishes selective cholesterol ester uptake from HDL.
Point Mutation
Point mutations can be introduced into genes like APOA1 to mimic naturally occurring variants that alter charge or conformation, affecting HDL clearance. CRISPR base editors or homology-directed repair with mutant donor templates can create precise amino acid substitutions. These models help dissect the structural determinants of HDL clearance regulation. For instance, mutating specific lysine residues on APOA1 alters its clearance rate in vivo.
Knock-in
Knock-in of tagged versions of SCARB1 or LRP1 (e.g., GFP or HA tags) allows real-time tracking of receptor trafficking and recycling in live cells. CRISPR knock-in using homology-directed repair can insert tags at the endogenous locus, preserving physiological regulation. These models are valuable for imaging endosomal trafficking of HDL receptors. Knock-in of human APOE isoforms into mouse models can also study HDL clearance in neurodegeneration.
Overexpression
CRISPR activation (CRISPRa) or lentiviral overexpression of SCARB1, LRP1, or APOA1 can test whether increased gene dosage enhances HDL clearance. Overexpression models are useful for gain-of-function studies and for identifying rate-limiting steps. For example, SR-BI overexpression in hepatocytes increases selective HDL cholesterol uptake. These models complement knockout studies to establish causality.
How EDITGENE Supports positive regulation of high-density lipoprotein particle clearance Research
Researchers studying positive regulation of high-density lipoprotein particle clearance-related genes often need to determine whether a candidate gene is causally involved in HDL uptake, trafficking, or degradation. EDITGENE provides a comprehensive suite of CRISPR-based services to generate precisely engineered cell models, enabling functional validation of genes identified from screens or genetic association studies.
Contact EDITGENE today to design your custom CRISPR model for positive regulation of high-density lipoprotein particle clearance research.
Frequently Asked Questions About positive regulation of high-density lipoprotein particle clearance
What is GO:0010983?
GO:0010983 is the Gene Ontology term for positive regulation of high-density lipoprotein particle clearance, a biological process that increases the rate of HDL removal from circulation [1,2].
What genes are involved in positive regulation of HDL clearance?
Key genes include SCARB1 (SR-BI), APOA1, LRP1, APOE, and ABCA1, which mediate receptor binding, endocytosis, and cholesterol efflux [2,7,8].
How is HDL particle clearance regulated?
HDL clearance is regulated by apolipoprotein charge and conformation, receptor expression levels, endocytic trafficking, and extracellular factors such as ethanol and hypoxia [1,2,4,5].
What diseases are associated with abnormal HDL clearance?
Dysregulated HDL clearance is linked to atherosclerosis, dyslipidemia, metabolic syndrome, graft-versus-host disease, and potentially neurodegeneration [3,4,7,8].
Which receptors mediate HDL clearance?
SR-BI (SCARB1) and LRP1 are major receptors that mediate HDL binding, selective cholesterol uptake, and endosomal trafficking [7,8].
How can CRISPR be used to study HDL clearance?
CRISPR knockout, knock-in, point mutation, and overexpression models allow functional dissection of genes involved in HDL clearance in hepatocyte cell lines and animal models [1,2,7,8].
What is the role of APOA1 in HDL clearance?
APOA1 is the major HDL apolipoprotein; its charge and conformation determine receptor binding and clearance rate in vivo.
Does alcohol affect HDL clearance?
Chronic alcohol consumption accelerates VLDL triglyceride turnover and upregulates HDL, potentially by increasing clearance of triglyceride-rich lipoproteins.
Is HDL clearance related to sleep apnea?
Obstructive sleep apnea is associated with dyslipidemia, and intermittent hypoxia may alter HDL clearance pathways.
What experimental models are used to study GO:0010983?
Common models include HepG2 cells, knockout mice, and CRISPR-engineered cell lines targeting SCARB1, LRP1, APOA1, and APOE [1,2,7,8].
Conclusion
GO:0010983, positive regulation of high-density lipoprotein particle clearance, is a critical biological process that governs plasma HDL levels and reverse cholesterol transport [1,2,8]. Its dysregulation contributes to cardiovascular and metabolic diseases, and it is modulated by genetic, lifestyle, and inflammatory factors [3,4,5,6]. Understanding the molecular mechanisms of HDL clearance regulation offers opportunities for therapeutic intervention. CRISPR-based gene editing provides powerful tools to dissect the causal roles of specific genes in this process [1,7,8]. EDITGENE's comprehensive services enable researchers to generate knockout, knock-in, point mutation, and overexpression models, accelerating discoveries in lipid metabolism and disease [1,2,7,8].
References
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- 3. Chagué C et al.. 2022. High-density lipoprotein infusion protects from acute graft-versus-host disease in experimental allogeneic hematopoietic cell transplantation.. Am J Transplant 22(5):1350-1361 PMID: 35038785
- 4. Barros D et al.. 2019. Obstructive sleep apnea and dyslipidemia: from animal models to clinical evidence.. Sleep 42(3) PMID: 30476296
- 5. Sane T et al.. 1984. Accelerated turnover of very low density lipoprotein triglycerides in chronic alcohol users. A possible mechanism for the up-regulation of high density lipoprotein by ethanol.. Atherosclerosis 53(2):185-93 PMID: 6517974
- 6. Ke J et al.. 2022. Exploring the Genetic Association between Obesity and Serum Lipid Levels Using Bivariate Methods.. Twin Res Hum Genet 25(6):234-244 PMID: 36606461
- 7. Laatsch A et al.. 2012. Low density lipoprotein receptor-related protein 1 dependent endosomal trapping and recycling of apolipoprotein E.. PLoS One 7(1):e29385 PMID: 22238606
- 8. van der Velde AE et al.. 2005. Shifting gears: liver SR-BI drives reverse cholesterol transport in macrophages.. J Clin Invest 115(10):2699-701 PMID: 16200207
