Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (430 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Lipid-protein complexes involved in the transportation and metabolism of lipids in the body. They are spherical particles consisting of a hydrophobic core of triglycerides and cholesterol esters surrounded by a layer of hydrophilic free cholesterol; phospholipids; and apolipoproteins. Lipoproteins are classified by their varying buoyant density and sizes.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Circulating Lipoproteins; Lipoproteins, Circulating; Lipoprotein.
Where it fits in the MeSH classification
- Broader topics
- Lipids; Proteins
- Narrower topics
- Apolipoproteins; ATP Binding Cassette Transporter, Subfamily G, Member 5; ATP Binding Cassette Transporter, Subfamily G, Member 8; Chylomicrons; Lipoprotein(a); Lipoprotein-X; Lipoproteins, HDL; Lipoproteins, IDL; Lipoproteins, LDL; Lipoproteins, VLDL
- See also
- Apolipoproteins; Hyperlipoproteinemias; Hypolipoproteinemias; Lipoid Proteinosis of Urbach and Wiethe; Proteolipids; Receptors, Lipoprotein; Lipid-Linked Proteins
Related concepts
Research landscape
PubMed indexes 173,798 records tagged with the MeSH heading “Lipoproteins” (counts retrieved 2026-10-31). 26,940 of them (15.5%) were published from 2020 onward, and the busiest period so far is through 1999 with 60,884 records.
Reviews account for 19,370 records (11.1%) and meta-analyses for 2,135. Randomized controlled trials number 9,712 (5.6%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 60,884 |
| 2000-2009 | 41,279 |
| 2010-2019 | 44,695 |
| 2020 onward | 26,940 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 19,370 | 11.1% |
| Meta-analyses | 2,135 | 1.2% |
| Randomized controlled trials | 9,712 | 5.6% |
Method: PubMed query "Lipoproteins"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Proteomic signatures of the APOE ε4 and APOE ε2 genetic variants and Alzheimer's disease | 2026 | Research article Design not recorded in structured metadata | 5 | cc by PMID 42141098 · DOI · PMC13190297 |
| Lipid Nanoparticle Protein Coronas Arise through Lipoprotein Fusion Rather Than Shell-like Adsorption | 2026 | Research article Design not recorded in structured metadata | 4 | cc by PMID 42677364 · DOI · PMC13523733 |
| Lipoprotein(a) and residual cardiovascular risks in Japanese patients with coronary artery disease who achieve guideline-recommended low-density lipoprotein cholesterol goals | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42177636 · DOI · PMC13696080 |
Proteomic signatures of the APOE ε4 and APOE ε2 genetic variants and Alzheimer's disease [1]
Abstract reading summary — source excerpts
- Opening excerpt
- The APOE locus is the strongest genetic factor for Alzheimer's disease, with ε4 increasing and ε2 decreasing risk, yet the basis of these opposing effects remains unclear.
- Closing excerpt
- Together, these findings reveal that APOE2 and APOE4 shape Alzheimer's disease risk through distinct molecular architectures and identify candidate biomarkers and targets for allele-specific interventions.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (149 words)
The APOE locus is the strongest genetic factor for Alzheimer's disease, with ε4 increasing and ε2 decreasing risk, yet the basis of these opposing effects remains unclear. Here we performed a multicohort proteomic analysis across plasma and cerebrospinal fluid in GNPC, BioFINDER-2, ADNI, UK BioBank, and PPMI. APOE-associated protein alterations are detectable before amyloid pathology and remain stable across age and disease progression. APOE2-associated proteins were enriched in pathways related to cellular maintenance and anti-inflammatory processes. By contrast, APOE4 showed a limited set of upstream mediators linked to cell-cycle and oligodendrocyte precursor cell biology, and a broader group of proteins reflecting vascular, immune, and proteostatic dysfunction shaped by downstream pathology. Comparative analyses highlighted allele-specific mediators and oppositely regulated proteins contributing to differential disease risk. Together, these findings reveal that APOE2 and APOE4 shape Alzheimer's disease risk through distinct molecular architectures and identify candidate biomarkers and targets for allele-specific interventions.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42141098 · DOI · PMC13190297
Lipid Nanoparticle Protein Coronas Arise through Lipoprotein Fusion Rather Than Shell-like Adsorption [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The protein corona influences the in vivo biodistribution of ionizable lipid nanoparticles (LNPs) in nucleic acid delivery, yet their structural architecture remains poorly defined.
- Closing excerpt
- Together, these findings support a model in which the biological identity of LNPs arises through membrane remodeling rather than shell-like adsorption and provide a framework for the rational design of targeted nanomedicines.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (142 words)
The protein corona influences the in vivo biodistribution of ionizable lipid nanoparticles (LNPs) in nucleic acid delivery, yet their structural architecture remains poorly defined. Using cryo-transmission electron microscopy, we visualized LNP-protein interactions in their native state. We show that, unlike the discrete "fuzzy" shells observed on hard nanoparticles, LNPs displayed no peripheral protein shell. Instead, controlled incubation and competitive "dual-particle" assays, supported by molecular dynamics simulations, indicate that LNP membranes undergo localized thickening and electron-dense remodeling consistent with lipoprotein integration rather than surface adsorption. Similar features were observed in extracellular vesicles, suggesting that this behavior is shared among lipid-based carriers, and proteomic analysis identified apolipoproteins as the dominant associated proteins. Together, these findings support a model in which the biological identity of LNPs arises through membrane remodeling rather than shell-like adsorption and provide a framework for the rational design of targeted nanomedicines.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42677364 · DOI · PMC13523733
Lipoprotein(a) and residual cardiovascular risks in Japanese patients with coronary artery disease who achieve guideline-recommended low-density lipoprotein cholesterol goals [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Background and aimsCurrent guidance recommends better LDL-C control in patients with elevated Lp(a) as Lp(a) lowering therapies are unavailable.
- Closing excerpt
- The Lp(a) threshold amongst Japanese patients with CAD at risk of recurrent events appears lower than in Caucasian populations which merits further evaluation.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (139 words)
Background and aimsCurrent guidance recommends better LDL-C control in patients with elevated Lp(a) as Lp(a) lowering therapies are unavailable. Whether risks attributable to Lp(a) are mitigated in patients with CAD who achieved LDL-C MethodsMulticentre retrospective observational study analysed 1581 Japanese patients with CAD [Lp(a)-JAPAN: jRCT1050260016]. Risk of MACE (cardiac-caused death + nonfatal MI + coronary revascularization in non-culprit segments) was compared according to Lp(a) levels (ResultsDuring the 5.1-year observation amongst patients with LDL-C ≥55mg/dL (n=1069), MACE occurred in 21.3% with risk of MACE increasing with Lp(a) levels (3.9, 7.9, and 11.0 events per 100 person-years for ConclusionsWhilst lower achieved LDL-C attenuates in part the risk from Lp(a), elevated Lp(a) levels still associate with worse cardiovascular outcomes. The Lp(a) threshold amongst Japanese patients with CAD at risk of recurrent events appears lower than in Caucasian populations which merits further evaluation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42177636 · DOI · PMC13696080
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Prevalence of cerebral amyloid pathology in persons without dementia: a meta-analysis [4]
- Research article Association Between Lowering LDL-C and Cardiovascular Risk Reduction Among Different Therapeutic Interventions: A Systematic Review and Meta-analysis [5]
- Research article Efficacy and safety of LDL-lowering therapy among men and women: meta-analysis of individual data from 174,000 participants in 27 randomised trials [6]
- Research article Baseline and on-statin treatment lipoprotein(a) levels for prediction of cardiovascular events: individual patient-data meta-analysis of statin outcome trials [7]
- Research article A meta-analysis of genome-wide association studies identifies multiple longevity genes [8]
- Research article Association Between Low-Density Lipoprotein Cholesterol-Lowering Genetic Variants and Risk of Type 2 Diabetes: A Meta-analysis [9]
References
- Lu L, Pichet Binette A, Hristovska I, Janelidze S, Smets B, Cumplido-Mayoral I, et al.. Proteomic signatures of the APOE ε4 and APOE ε2 genetic variants and Alzheimer's disease. . 2026. PMID 42141098 · DOI · PMC13190297
- Grumelot S, Mohammed N, Yerima G, Colonrosado J, Sadeghi SA, Fang F, et al.. Lipid Nanoparticle Protein Coronas Arise through Lipoprotein Fusion Rather Than Shell-like Adsorption. . 2026. PMID 42677364 · DOI · PMC13523733
- Kataoka Y, Ray KK, Nicholls SJ, Katasako-Yabumoto A, Kitahara S, Hosoda H, et al.. Lipoprotein(a) and residual cardiovascular risks in Japanese patients with coronary artery disease who achieve guideline-recommended low-density lipoprotein cholesterol goals. . 2026. PMID 42177636 · DOI · PMC13696080
- Jansen WJ, Ossenkoppele R, Knol DL, Tijms BM, Scheltens P, Verhey FR, et al.. Prevalence of cerebral amyloid pathology in persons without dementia: a meta-analysis. JAMA. 2015. PMID 25988462 · DOI · PMC4486209
- Silverman MG, Ference BA, Im K, Wiviott SD, Giugliano RP, Grundy SM, et al.. Association Between Lowering LDL-C and Cardiovascular Risk Reduction Among Different Therapeutic Interventions: A Systematic Review and Meta-analysis. JAMA. 2016. PMID 27673306 · DOI
- Cholesterol Treatment Trialists' (CTT) Collaboration, Fulcher J, O'Connell R, Voysey M, Emberson J, Blackwell L, et al.. Efficacy and safety of LDL-lowering therapy among men and women: meta-analysis of individual data from 174,000 participants in 27 randomised trials. Lancet. 2015. PMID 25579834 · DOI
- Willeit P, Ridker PM, Nestel PJ, Simes J, Tonkin AM, Pedersen TR, et al.. Baseline and on-statin treatment lipoprotein(a) levels for prediction of cardiovascular events: individual patient-data meta-analysis of statin outcome trials. Lancet. 2018. PMID 30293769 · DOI
- Deelen J, Evans DS, Arking DE, Tesi N, Nygaard M, Liu X, et al.. A meta-analysis of genome-wide association studies identifies multiple longevity genes. Nat Commun. 2019. PMID 31413261 · DOI · PMC6694136
- Lotta LA, Sharp SJ, Burgess S, Perry JRB, Stewart ID, Willems SM, et al.. Association Between Low-Density Lipoprotein Cholesterol-Lowering Genetic Variants and Risk of Type 2 Diabetes: A Meta-analysis. JAMA. 2016. PMID 27701660 · DOI · PMC5386134
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.