Evidence map›Paper›PMID 42868980›Full record

ArticleJACC. Basic to translational science2026

A Chemokine Profile Linked to Both Triglyceride-Rich Lipoproteins and Lipoprotein(a), But Not LDL, Is Associated With Cardiovascular Disease.

Elias Björnson, Martin Adiels, Jakub Morze, Florentina Porsch, Anders Gummesson, Christoph J Binder, Clemens Wittenbecher, Chris J Packard, Jan Borén

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in JACC. Basic to translational science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Elias BjörnsonDepartment of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, Gothenburg, Sweden. Electronic address: https://twitter.com/EliasBjornson.
Martin AdielsDepartment of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, Gothenburg, Sweden; School of Public Health and Community Medicine, Institute of Medicine, University of Gothenburg, Gothenburg, Sweden.
Jakub MorzeDepartment of Life Sciences, SciLifeLab, Chalmers University of Technology, Gothenburg, Sweden.
Florentina PorschDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
Anders GummessonDepartment of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, Gothenburg, Sweden; Department of Clinical Genetics, Region Västra Götaland, Sahlgrenska University Hospital, Gothenburg, Sweden.
Christoph J BinderDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
Clemens WittenbecherDepartment of Life Sciences, SciLifeLab, Chalmers University of Technology, Gothenburg, Sweden.
Chris J PackardInstitute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom.
Jan BorénDepartment of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, Gothenburg, Sweden. Electronic address: jan.boren@wlab.gu.se.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Triglyceride-rich lipoproteins (TRL) and lipoprotein(a) [Lp(a)] demonstrate heightened per-particle atherogenicity compared with low-density lipoproteins (LDL), yet mechanistic underpinnings remain unclear. Using Mendelian randomization in >46,000 UK Biobank participants, we linked genetically determined variation in TRL/remnants, LDL, and Lp(a) to 2,920 plasma proteins and found causal associations with 432, 58, and 111 proteins, respectively. Notably, TRL/remnants and Lp(a) both impacted chemokine-signaling and leukocyte-chemotaxis pathways, distinct from LDL's effect on lipid metabolism. A specific chemokine signature linked to both TRL and Lp(a) accounted for around 40% (with wide confidence limits) of the TRL/remnant cholesterol: cardiovascular disease (CVD) association. However, a more general causal relationship between plasma chemokine concentrations and CVD risk independent of a TRL/Lp(a) effect was not supported by quantitative trait loci analysis. These results are compatible with a model in which TRL/Lp(a)-driven chemokine activation contributes meaningfully to CVD risk.

Indexed as

Cardiovascular diseaseinflammationLDLLp(a)Mendelian randomizationTRLsUK Biobank

Identifiers

PMID42868980
PMCPMC13685006

What OpenQuestion holds

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Registered trials

None linked

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.