Evidence map›Paper›PMID 38753254›Full record

ReviewCurrent atherosclerosis reports2024

Comparative Analysis of Atherogenic Lipoproteins L5 and Lp(a) in Atherosclerotic Cardiovascular Disease.

Omer Akyol, Chao-Yuh Yang, Darren G Woodside, Huan-Hsing Chiang, Chu-Huang Chen, Antonio M Gotto

Abstract readReviewComparative Study
In one paragraph

Review in Current atherosclerosis reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. 2025 Egyptian guidelines for the management of dyslipidemia.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2026
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Atherogenic circulating lipoproteins in ischemic stroke.Frontiers in cardiovascular medicine · 2024
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Omer AkyolMolecular Cardiology Research Laboratories, Vascular and Medicinal Research, The Texas Heart Institute, Houston, Texas, 77030, USA.
Chao-Yuh YangDepartment of Medicine, Baylor College of Medicine, One Baylor Plaza, Houston, Texas, 77030, USA.
Darren G WoodsideMolecular Cardiology Research Laboratories, The Texas Heart Institute, Houston, TX, 77030, USA.
Huan-Hsing ChiangMolecular Cardiology Research Laboratories, Vascular and Medicinal Research, The Texas Heart Institute, Houston, Texas, 77030, USA.
Chu-Huang ChenMolecular Cardiology Research Laboratories, Vascular and Medicinal Research, The Texas Heart Institute, Houston, Texas, 77030, USA. cchen@texasheart.org.
Antonio M GottoWeill Cornell Medical College, New York, NY, 10021, USA. amg2004@med.cornell.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewLow-density lipoprotein (LDL) poses a risk for atherosclerotic cardiovascular disease (ASCVD). As LDL comprises various subtypes differing in charge, density, and size, understanding their specific impact on ASCVD is crucial. Two highly atherogenic LDL subtypes-electronegative LDL (L5) and Lp(a)-induce vascular cell apoptosis and atherosclerotic changes independent of plasma cholesterol levels, and their mechanisms warrant further investigation. Here, we have compared the roles of L5 and Lp(a) in the development of ASCVD. RECENT

findingsLp(a) tends to accumulate in artery walls, promoting plaque formation and potentially triggering atherosclerosis progression through prothrombotic or antifibrinolytic effects. High Lp(a) levels correlate with calcific aortic stenosis and atherothrombosis risk. L5 can induce endothelial cell apoptosis and increase vascular permeability, inflammation, and atherogenesis, playing a key role in initiating atherosclerosis. Elevated L5 levels in certain high-risk populations may serve as a distinctive predictor of ASCVD. L5 and Lp(a) are both atherogenic lipoproteins contributing to ASCVD through distinct mechanisms. Lp(a) has garnered attention, but equal consideration should be given to L5.

Indexed as

AtherosclerosisLipoprotein(a)AnimalsApoptosisHumansLipoproteins, LDLLipoprotein(a)Lipoproteins, LDLAtherogenesisAtherosclerotic Cardiovascular DiseaseElectronegative LDLL5Lp(a)Oxidized LDL

Identifiers

PMID38753254
PMCPMC11192678

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Registered trials

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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.