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Hyperlipidemia

Disease Pathophysiology Research Template

2026-03-03
Falcon MONDO:0021187 Model: Edison Scientific Literature 38 citations

Question: You are an expert researcher providing comprehensive, well-cited information.

Provide detailed information focusing on: 1. Key concepts and definitions with current understanding 2. Recent developments and latest research (prioritize 2023-2024 sources) 3. Current applications and real-world implementations 4. Expert opinions and analysis from authoritative sources 5. Relevant statistics and data from recent studies

Format as a comprehensive research report with proper citations. Include URLs and publication dates where available. Always prioritize recent, authoritative sources and provide specific citations for all major claims.

Disease Pathophysiology Research Template

Target Disease

  • Disease Name: Hyperlipidemia
  • MONDO ID: (if available)
  • Category: Complex

Research Objectives

Please provide a comprehensive research report on the pathophysiology of Hyperlipidemia. Focus on the molecular and cellular mechanisms underlying disease progression.

Required Information

1. Core Pathophysiology

  • What are the primary pathophysiological mechanisms?
  • What molecular pathways are dysregulated?
  • What cellular processes are affected?

2. Key Molecular Players

  • Genes/Proteins: Which genes are causally involved or implicated?
  • Chemical Entities: What metabolites, drugs, or small molecules are relevant?
  • Cell Types: Which cell types are primarily affected?
  • Anatomical Locations: Which tissues/organs are involved?

3. Biological Processes (for GO annotation)

  • What biological processes (GO terms) are disrupted?
  • Consider: signaling pathways, metabolic processes, cellular responses, transport, etc.

4. Cellular Components

  • Where in the cell do key processes occur?
  • Consider: organelles, membrane compartments, extracellular space, etc.

5. Disease Progression

  • What is the sequence of events from initial trigger to clinical manifestation?
  • Are there distinct stages or phases?

6. Phenotypic Manifestations

  • What are the key clinical phenotypes?
  • How do they relate to the underlying mechanisms?

Citation Requirements

  • Cite primary literature (PMID preferred) for all mechanistic claims
  • Prioritize recent reviews and landmark papers
  • Include direct quotes where possible to support key statements

Output Format

Structure your response as a narrative that could be used to populate a disease knowledge base entry with: - Pathophysiology description - Gene/protein annotations with ontology terms (HGNC, GO) - Phenotype associations (HP terms) - Cell type involvement (CL terms) - Anatomical locations (UBERON terms) - Chemical entities (CHEBI terms) - Evidence items with PMIDs

Pathophysiology Research Report: Hyperlipidemia (Complex)

Disease identifiers

1) Key concepts and definitions (current understanding)

Hyperlipidemia is a disorder of elevated circulating lipids and/or lipoproteins, commonly manifesting as increased apoB-containing atherogenic particles (LDL, VLDL remnants) and/or triglyceride-rich lipoproteins (TRLs) (VLDL, chylomicrons and remnants). Mechanistically, hyperlipidemia reflects imbalance among (i) hepatic/intestinal lipoprotein production, (ii) intravascular lipolysis and remodeling, and (iii) hepatic clearance by receptor-mediated pathways; downstream, excess apoB particles drive arterial wall retention, oxidation, foam-cell formation, and inflammation.

A key contemporary refinement is the concept of residual lipid risk: even after intensive LDL-C lowering, TRLs/remnants, Lp(a), and impaired cholesterol efflux can sustain atherothrombotic risk. This is emphasized in recent hypertriglyceridemia syntheses reporting LDL-C–independent residual risk from elevated TG/TRLs (scicchitano2024hypertriglyceridemiamolecularand pages 1-2).

2) Core pathophysiology (molecular pathways and dysregulated cellular processes)

2.1 ApoB/LDL axis: impaired clearance + vascular retention

LDLR–PCSK9 axis (hepatic clearance): PCSK9 regulates circulating LDL-C primarily by promoting LDL receptor (LDLR) degradation. A 2024 primary mechanistic study in Nature Communications summarizes the canonical concept: “PCSK9 binds to and degrades low-density lipoprotein (LDL) receptor, leading to increase of LDL cholesterol in blood” (published 2024-03; https://doi.org/10.1038/s41467-024-46336-2) (shin2024pcsk9stimulatessyk pages 1-2).

Arterial wall injury initiation: Excess LDL-C contributes to foam-cell formation and plaque inflammation; the same study notes: “Excessive LDL-C in the blood infiltrates the sub-endothelial layer and is oxidized… resulting in foam cell formation, vascular inflammation, and atherosclerosis” (shin2024pcsk9stimulatessyk pages 1-2).

2.2 LDLR-independent inflammatory signaling by PCSK9 (newer mechanistic insight)

A major 2024 development is evidence that PCSK9 can promote vascular inflammation independently of LDLR, via a receptor/signaling complex in immune and vascular cells. Shin et al. report: “PCSK9 itself directly induces inflammation and aggravates atherosclerosis independently of the LDL receptor” and identify CAP1 as the binding partner: “CAP1 is the main binding partner of PCSK9…” with downstream mediators “Syk” and “PKCδ” and NF-κB activation (shin2024pcsk9stimulatessyk pages 1-2).

They further connect PCSK9→CAP1 to innate immune patterning and lipid uptake: PCSK9/CAP1 signaling includes “induction of cytokines, Toll like receptor 4, and scavenger receptors, enhancing the uptake of oxidized LDL” (shin2024pcsk9stimulatessyk pages 1-2). Dose-response evidence is shown in human monocytes/endothelial cells: “rhPCSK9… induced p65 phosphorylation… in a dose-dependent manner” and increased inflammatory cytokine transcripts (TNF-α, IL-1β, IL-6) and adhesion molecules (VCAM1, ICAM1, SELE) (shin2024pcsk9stimulatessyk pages 2-3).

Implication: Hyperlipidemia pathophysiology is not purely a “lipid transport” disorder; in at least some contexts it includes a feed-forward immunometabolic loop in which lipid-regulatory proteins (e.g., PCSK9) directly modulate vascular inflammation.

2.3 TRL/TG axis: overproduction, impaired lipolysis, impaired remnant clearance

TRL metabolism: TRLs are primarily VLDL (liver-derived) and chylomicrons (intestine-derived), which deliver triglycerides to tissues and are converted to remnants via lipoprotein lipase (LPL) and other enzymes. Chen et al. (2024-01; https://doi.org/10.1186/s12944-023-01993-y) summarize that this regulation is “predominantly governed by ANGPTL4/3/8” (chen2024unlockingthemysteries pages 1-2).

ApoC-III as a central inhibitor of TRL clearance: Multiple recent sources converge that APOC3/apoC-III inhibits LPL-mediated lipolysis and suppresses hepatic remnant clearance. - Mechanistic definition (review): “ApoC-III is a well-known inhibitor of LPL” and contributes to decreased VLDL clearance in hypertriglyceridemia via an apoC-III–dominated TRL state (Giammanco et al., 2023-01-23 online; https://doi.org/10.1007/s11883-023-01080-8) (giammanco2023apociiiagatekeeper pages 1-2). - Concise mechanism (trial intro): “ApoC-III downregulates lipoprotein metabolism by inhibiting lipoprotein and hepatic lipases and by reducing hepatic uptake of TRLs via low-density lipoprotein (LDL) and LDL receptor-related protein receptors” (Karwatowska‑Prokopczuk et al., 2024-10; https://doi.org/10.1186/s12944-024-02297-5) (karwatowskaprokopczuk2024efficacyandsafety pages 1-2).

VLDL assembly/biogenesis (intracellular lipidation pathway): Hepatic VLDL secretion depends on apoB availability and ER lipidation. - “The biosynthesis of VLDL is a multistep process that begins in the rough endoplasmic reticulum (RER)” (chen2024unlockingthemysteries pages 1-2). - “Hepatic VLDL assembly starts with the cotranslational translocation of APOB… where microsomal triglyceride transfer protein (MTP) helps in the first lipid decoration of APOB” (chen2024unlockingthemysteries pages 1-2). - “Without sufficient lipidation, nascent APOB is degraded” (chen2024unlockingthemysteries pages 1-2).

These steps represent actionable nodes for therapy (e.g., MTP inhibition; apoB synthesis inhibition; ANGPTL3 inhibition) (chen2024unlockingthemysteries pages 1-2).

2.4 Foam cell biology and impaired reverse cholesterol transport (RCT)

Atherogenesis emerges when cholesterol uptake exceeds efflux in vascular cells—especially macrophages. Albitar et al. (2024-07; https://doi.org/10.3390/nu16132156) describe macrophage foam-cell formation and intracellular handling: - “Lipids engulfed through phagocytosis… [enter] lysosomes. Lysosomes break down cholesteryl esters to release free cholesterol. This free cholesterol is then… modified by… ACAT1… reserved inside the cell, particularly in the ER” (albitar2024effectsoflipoproteins pages 5-7). - In lesions, “Following the development of atherosclerosis, elevated levels of ACAT1 and reduced expression of NCEH result in the macrophage’s overload with cholesterol” (albitar2024effectsoflipoproteins pages 5-7).

They also situate RCT as a protective pathway controlled by nuclear receptor/transporter programs: “RCT… is controlled by the X receptor (LXR) of the liver, along with… ABCA1 and ABCG1” (albitar2024effectsoflipoproteins pages 5-7).

3) Key molecular players (genes/proteins), cell types, and tissues

3.1 Gene/protein annotations (HGNC symbols; selected)

Core LDL/apoB metabolism and clearance - LDLR (low density lipoprotein receptor): hepatic endocytosis/clearance of LDL; genetically implicated in familial hypercholesterolemia (FH) (abbasi2024newinsightsinto pages 1-2). - PCSK9: promotes LDLR degradation; additionally promotes LDLR-independent inflammation via CAP1→Syk/PKCδ→NF-κB (shin2024pcsk9stimulatessyk pages 1-2, shin2024pcsk9stimulatessyk pages 2-3). - APOB: structural protein of VLDL/LDL; required for VLDL assembly and secretion; dependent on MTP-mediated lipidation (chen2024unlockingthemysteries pages 1-2). - MTTP (MTP): microsomal triglyceride transfer protein; lipidates apoB in the ER during VLDL biogenesis (chen2024unlockingthemysteries pages 1-2).

Core TRL/TG metabolism - LPL: hydrolyzes TG in TRLs (contextualized as central regulator in ApoC-III review) (giammanco2023apociiiagatekeeper pages 1-2). - APOC3: inhibits LPL and reduces hepatic uptake of TRLs via LDLR/LRP receptors; shifts TRL clearance kinetics toward slower, apoC-III–dominated clearance in hypertriglyceridemia (karwatowskaprokopczuk2024efficacyandsafety pages 1-2, giammanco2023apociiiagatekeeper pages 1-2). - ANGPTL3/ANGPTL4/ANGPTL8: regulators of TRL metabolism and LPL activity (chen2024unlockingthemysteries pages 1-2).

Cholesterol efflux/foam-cell biology - ABCA1, ABCG1 (ATP-binding cassette transporters): cholesterol efflux in RCT program under LXR control (albitar2024effectsoflipoproteins pages 5-7). - ACAT1 (acetyl-CoA acetyltransferase 1; SOAT1 commonly used synonym in lipid literature): re-esterifies free cholesterol in ER, promoting cholesterol storage/foam phenotype when dysregulated (albitar2024effectsoflipoproteins pages 5-7).

3.2 Cell types (CL) most implicated

3.3 Anatomical locations (UBERON)

3.4 Chemical entities (CHEBI; examples relevant to mechanisms)

4) Biological processes (GO) and cellular components (GO CC) disrupted (knowledge-base oriented)

GO Biological Process (selected, pathophysiology-aligned)

GO Cellular Component (selected)

5) Disease progression model (sequence from trigger to clinical manifestation)

  1. Initiating drivers: genetic variants (e.g., LDLR/APOB/PCSK9; APOC3; LPL pathway genes) and/or metabolic drivers (insulin resistance, diet, obesity) increase apoB particle production and/or impair clearance (abbasi2024newinsightsinto pages 1-2, giammanco2023apociiiagatekeeper pages 1-2).
  2. Overproduction / impaired processing:
  3. Hepatic VLDL production increases when apoB is lipidated efficiently; apoB that is insufficiently lipidated is degraded, linking secretion to intrahepatic lipid availability and MTP function (chen2024unlockingthemysteries pages 1-2).
  4. TRL hydrolysis is slowed when APOC3 is high and when ANGPTL regulators inhibit lipolysis (karwatowskaprokopczuk2024efficacyandsafety pages 1-2, chen2024unlockingthemysteries pages 1-2).
  5. Particle persistence and arterial entry: Excess apoB particles infiltrate subendothelial space; oxidation occurs in ROS-rich environments involving macrophages/ECs/SMCs, promoting foam cells and inflammation (shin2024pcsk9stimulatessyk pages 1-2).
  6. Foam-cell formation and defective efflux: macrophage uptake of modified lipoproteins drives lysosomal hydrolysis and ER re-esterification; increased ACAT1 and reduced NCEH promote cholesterol ester accumulation and foam phenotype; RCT dysfunction limits protective efflux (albitar2024effectsoflipoproteins pages 5-7).
  7. Inflammation amplification:
  8. Lipid-driven sterile inflammation proceeds via cytokines and adhesion molecule induction.
  9. PCSK9 may amplify inflammation independently of LDLR via CAP1 and NF-κB pathway activation, increasing TLR4/scavenger receptor expression and oxLDL uptake (shin2024pcsk9stimulatessyk pages 1-2, shin2024pcsk9stimulatessyk pages 2-3).
  10. Clinical manifestations: ASCVD events (MI, stroke, PAD), valve disease and arterial stenosis in severe familial disease; pancreatitis in severe hypertriglyceridemia/chylomicronemia (abbasi2024newinsightsinto pages 1-2, guan2024lipoproteinapheresisan pages 2-5, karwatowskaprokopczuk2024efficacyandsafety pages 1-2).

6) Phenotypic manifestations (HP; examples) and mechanistic links

Major clinical phenotypes (examples; mapable to HPO)

Quantitative phenotype-linked thresholds and risk

7) Recent developments (prioritizing 2023–2024)

7.1 PCSK9 biology expanded beyond LDLR recycling

The 2024 Nature Communications work extends PCSK9 from LDLR degradation into direct inflammatory signaling: “PCSK9 itself directly induces inflammation… independently of the LDL receptor” (shin2024pcsk9stimulatessyk pages 1-2) and mechanistically ties to CAP1 and NF-κB phosphorylation/cytokine induction (shin2024pcsk9stimulatessyk pages 2-3). This helps explain why PCSK9 modulation could influence plaque biology beyond LDL-C reduction.

7.2 Next-generation TRL therapeutics targeting ApoC-III

ApoC-III targeting is now supported by human early-phase data. In a phase 1 trial, olezarsen (GalNAc3-conjugated hepatic-targeted ASO) significantly reduced apoC-III and triglycerides: in multiple-dose cohort, “percentage reduction in apoC-III/TG was −81.6/−73.8%” at day 92 versus placebo reductions (published 2024-10; https://doi.org/10.1186/s12944-024-02297-5) (karwatowskaprokopczuk2024efficacyandsafety pages 1-2). The study also explicitly frames clinical relevance to pancreatitis: FCS is “primarily associated with pancreatitis” and severe HTG associated with both pancreatitis and CVD (karwatowskaprokopczuk2024efficacyandsafety pages 1-2).

7.3 LDLR-independent lipid lowering via ANGPTL3 inhibition

Evinacumab (anti-ANGPTL3) is described as an FDA-approved therapy for HoFH that lowers LDL-C via “an LDL receptor–independent mechanism” with a case report showing 53.4% time-averaged LDL-C reduction after 12 months (published 2023-05; https://doi.org/10.1210/jcemcr/luad058) (chen2024unlockingthemysteries pages 10-11).

7.4 Increased emphasis on VLDL/TRL production and trafficking as causal targets

A 2024 conceptual review highlights VLDL (precursor of LDL) and notes that interventions targeting VLDL production or metabolism “independent of the LDL receptor” may decrease cholesterol levels and provide benefits beyond LDL-centric therapy (chen2024unlockingthemysteries pages 1-2). Figures summarizing these pathways are provided in the paper (Fig. 2 and Fig. 3) (chen2024unlockingthemysteries media aecdd5d3, chen2024unlockingthemysteries media 24e615f7).

8) Current applications and real-world implementations (guidelines/position papers and clinical practice)

8.1 LDL-C goal attainment remains poor (implementation gap)

8.2 Clinical implementation examples (real-world)

9) Relevant statistics and recent study data (selected)

Disease burden and care gaps

TRL/TG risk

Effect sizes for emerging therapies

10) Expert opinion synthesis (authoritative sources)

Recent expert position papers emphasize that LDL-C lowering remains foundational (“lower is better for longer” and “earlier the better”), but that real-world attainment is inadequate and that combination and next-generation therapies are needed for high-risk groups (banach20242024recommendationson pages 1-2). Complementary diagnostic guidelines stress standardized lipid profiling and expanded targets (e.g., non-HDL-C, remnants/small dense LDL) to improve early detection and monitoring (solnica20242024guidelinesof pages 1-2).

11) Knowledge-base-ready structured annotations

11.1 Entity summary table (mechanism-centered)

Table (click to expand)
Module Key HGNC genes/proteins Core mechanism (1–2 lines) Key cell types (CL) Key tissues (UBERON) Key cellular components Evidence
LDL-C/apoB clearance LDLR, PCSK9 PCSK9 promotes LDLR degradation, raising LDL-C; LDL infiltrates subendothelium → oxidation → foam cells/inflammation hepatocyte; monocyte/macrophage; EC; SMC liver; artery plasma membrane; extracellular space Shin 2024 Nat Commun (doi:10.1038/s41467-024-46336-2) (shin2024pcsk9stimulatessyk pages 1-2)
PCSK9 inflammatory signaling (LDLR-independent) PCSK9, CAP1, SYK, PRKCD (PKCδ), NFKB (p65), TLR4 PCSK9–CAP1 binding activates Syk/PKCδ and NF-κB, induces cytokines/adhesion molecules, increases scavenger receptors and oxLDL uptake monocyte/macrophage; EC artery; immune system plasma membrane; cytosol/nucleus Shin 2024 (shin2024pcsk9stimulatessyk pages 1-2, shin2024pcsk9stimulatessyk pages 2-3)
TRL/TG metabolism APOC3, LPL, ANGPTL3/4/8 ANGPTL3/4/8 regulate TRL processing; ApoC-III inhibits LPL and reduces hepatic TRL uptake via LDLR/LRP receptors hepatocyte; adipocyte; myocyte; macrophage liver; adipose; muscle capillary lumen/extracellular; lipoprotein particles Chen 2024 (doi:10.1186/s12944-023-01993-y) (chen2024unlockingthemysteries pages 1-2); Karwatowska‑Prokopczuk 2024 (karwatowskaprokopczuk2024efficacyandsafety pages 1-2); Giammanco 2023 (giammanco2023apociiiagatekeeper pages 1-2)
VLDL production/trafficking APOB, MTTP VLDL assembly begins in rough ER; MTP lipidates apoB; insufficient lipidation → apoB degradation; secretion drives TRL burden hepatocyte liver rough ER; secretory pathway Chen 2024 (chen2024unlockingthemysteries pages 1-2); Fig. 2 visual (chen2024unlockingthemysteries media aecdd5d3)
Foam cells & RCT LXR, ABCA1, ABCG1, APOE, ACAT1 Lysosomal CE hydrolysis → free cholesterol; ER re-esterification via ACAT1; transporter downregulation with scavenger receptor upregulation → foam cells; RCT under LXR/ABCA1/ABCG1 macrophage; vascular cells arterial intima; liver lysosome; ER; plasma membrane Albitar 2024 Nutrients (doi:10.3390/nu16132156) (albitar2024effectsoflipoproteins pages 5-7)

11.2 Drugs/chemical interventions linked to mechanisms (examples)

12) Evidence items (with identifiers)

Note: Many journal excerpts retrieved here include DOI/URL and dates but not PMIDs in-text; where PMIDs are not present in the retrieved content, DOI/URL-based citation is provided.

  1. Shin D, et al. PCSK9 stimulates Syk, PKCδ, and NF-κB… independently of LDL receptor. Nature Communications. Accepted 2024-02-23. DOI/URL: https://doi.org/10.1038/s41467-024-46336-2. Key quote: “PCSK9 itself directly induces inflammation…” (shin2024pcsk9stimulatessyk pages 1-2, shin2024pcsk9stimulatessyk pages 2-3).
  2. Chen J, et al. Unlocking the mysteries of VLDL. Lipids in Health and Disease. 2024-01. DOI/URL: https://doi.org/10.1186/s12944-023-01993-y. Key quote: VLDL assembly begins in rough ER; MTP lipidates apoB (chen2024unlockingthemysteries pages 1-2). Figures summarizing pathways (chen2024unlockingthemysteries media aecdd5d3, chen2024unlockingthemysteries media 24e615f7).
  3. Giammanco A, et al. APOC-III: a Gatekeeper. Current Atherosclerosis Reports. Published online 2023-01-23. DOI/URL: https://doi.org/10.1007/s11883-023-01080-8. Key quote: “ApoC-III is a well-known inhibitor of LPL…” (giammanco2023apociiiagatekeeper pages 1-2).
  4. Albitar O, et al. Effects of Lipoproteins on Metabolic Health. Nutrients. 2024-07. DOI/URL: https://doi.org/10.3390/nu16132156. Key quote: lysosomal CE hydrolysis, ACAT1 re-esterification in ER, foam cell overload with high ACAT1/low NCEH (albitar2024effectsoflipoproteins pages 5-7).
  5. Karwatowska‑Prokopczuk E, et al. Olezarsen phase 1. Lipids in Health and Disease. 2024-10. DOI/URL: https://doi.org/10.1186/s12944-024-02297-5. Quantitative reductions in apoC-III/TG and thresholds defining SHTG (karwatowskaprokopczuk2024efficacyandsafety pages 1-2).
  6. Banach M, et al. ILEP position paper. Drugs. Published online 2024-11-04. DOI/URL: https://doi.org/10.1007/s40265-024-02105-5. LDL-C goal attainment gaps (banach20242024recommendationson pages 1-2).

References

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  5. (chen2024unlockingthemysteries pages 1-2): Jingfei Chen, Zhenfei Fang, Qin Luo, Xiao Wang, Mohamad Warda, Avash Das, Federico Oldoni, and Fei Luo. Unlocking the mysteries of vldl: exploring its production, intracellular trafficking, and metabolism as therapeutic targets. Lipids in Health and Disease, Jan 2024. URL: https://doi.org/10.1186/s12944-023-01993-y, doi:10.1186/s12944-023-01993-y. This article has 47 citations and is from a peer-reviewed journal.

  6. (giammanco2023apociiiagatekeeper pages 1-2): Antonina Giammanco, Rossella Spina, Angelo B. Cefalù, and Maurizio Averna. Apoc-iii: a gatekeeper in controlling triglyceride metabolism. Current Atherosclerosis Reports, 25:67-76, Jan 2023. URL: https://doi.org/10.1007/s11883-023-01080-8, doi:10.1007/s11883-023-01080-8. This article has 75 citations and is from a peer-reviewed journal.

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  11. (banach20242024recommendationson pages 1-2): Maciej Banach, Željko Reiner, Stanisław Surma, Gani Bajraktari, Agata Bielecka-Dabrowa, Matjaz Bunc, Ibadete Bytyçi, Richard Ceska, Arrigo F. G. Cicero, Dariusz Dudek, Krzysztof Dyrbuś, Jan Fedacko, Zlatko Fras, Dan Gaita, Dov Gavish, Marek Gierlotka, Robert Gil, Ioanna Gouni-Berthold, Piotr Jankowski, Zoltán Járai, Jacek Jóźwiak, Niki Katsiki, Gustavs Latkovskis, Stefania Lucia Magda, Eduard Margetic, Roman Margoczy, Olena Mitchenko, Azra Durak-Nalbantic, Petr Ostadal, Gyorgy Paragh, Zaneta Petrulioniene, Francesco Paneni, Ivan Pećin, Daniel Pella, Arman Postadzhiyan, Anca Pantea Stoian, Matias Trbusic, Cristian Alexandru Udroiu, Margus Viigimaa, Dragos Vinereanu, Charalambos Vlachopoulos, Michal Vrablik, Dusko Vulic, and Peter E. Penson. 2024 recommendations on the optimal use of lipid-lowering therapy in established atherosclerotic cardiovascular disease and following acute coronary syndromes: a position paper of the international lipid expert panel (ilep). Drugs, 84:1541-1577, Nov 2024. URL: https://doi.org/10.1007/s40265-024-02105-5, doi:10.1007/s40265-024-02105-5. This article has 51 citations and is from a domain leading peer-reviewed journal.

  12. (chen2024unlockingthemysteries pages 10-11): Jingfei Chen, Zhenfei Fang, Qin Luo, Xiao Wang, Mohamad Warda, Avash Das, Federico Oldoni, and Fei Luo. Unlocking the mysteries of vldl: exploring its production, intracellular trafficking, and metabolism as therapeutic targets. Lipids in Health and Disease, Jan 2024. URL: https://doi.org/10.1186/s12944-023-01993-y, doi:10.1186/s12944-023-01993-y. This article has 47 citations and is from a peer-reviewed journal.

  13. (chen2024unlockingthemysteries media aecdd5d3): Jingfei Chen, Zhenfei Fang, Qin Luo, Xiao Wang, Mohamad Warda, Avash Das, Federico Oldoni, and Fei Luo. Unlocking the mysteries of vldl: exploring its production, intracellular trafficking, and metabolism as therapeutic targets. Lipids in Health and Disease, Jan 2024. URL: https://doi.org/10.1186/s12944-023-01993-y, doi:10.1186/s12944-023-01993-y. This article has 47 citations and is from a peer-reviewed journal.

  14. (chen2024unlockingthemysteries media 24e615f7): Jingfei Chen, Zhenfei Fang, Qin Luo, Xiao Wang, Mohamad Warda, Avash Das, Federico Oldoni, and Fei Luo. Unlocking the mysteries of vldl: exploring its production, intracellular trafficking, and metabolism as therapeutic targets. Lipids in Health and Disease, Jan 2024. URL: https://doi.org/10.1186/s12944-023-01993-y, doi:10.1186/s12944-023-01993-y. This article has 47 citations and is from a peer-reviewed journal.

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