A Chemokine Profile Linked to Both Triglyceride-Rich Lipoproteins and Lipoprotein(a), But Not LDL, Is Associated With Cardiovascular Disease.
7 affiliations
- 1Department of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, Gothenburg, Sweden. Electronic address: https://twitter.com/EliasBjornson.
- 2Department 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.
- 3Department of Life Sciences, SciLifeLab, Chalmers University of Technology, Gothenburg, Sweden.
- 4Department of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
- 5Department 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.
- 6Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom.
- 7Department of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, Gothenburg, Sweden. Electronic address: [email protected].
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.
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BibTeX
@article{bjornson2026chemokine,
title = {{A Chemokine Profile Linked to Both Triglyceride-Rich Lipoproteins and Lipoprotein(a), But Not LDL, Is Associated With Cardiovascular Disease.}},
author = {Elias Björnson and Martin Adiels and Jakub Morze and Florentina Porsch and Anders Gummesson and Christoph J Binder and Clemens Wittenbecher and Chris J Packard and Jan Borén},
journal = {JACC. Basic to translational science},
year = {2026},
month = oct,
doi = {10.1016/j.jacbts.2026.101736},
url = {https://europepmc.org/article/MED/42868980},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - A Chemokine Profile Linked to Both Triglyceride-Rich Lipoproteins and Lipoprotein(a), But Not LDL, Is Associated With Cardiovascular Disease.
AU - Elias Björnson
AU - Martin Adiels
AU - Jakub Morze
AU - Florentina Porsch
AU - Anders Gummesson
AU - Christoph J Binder
AU - Clemens Wittenbecher
AU - Chris J Packard
AU - Jan Borén
PY - 2026
DA - 2026/10/13
JO - JACC. Basic to translational science
DO - 10.1016/j.jacbts.2026.101736
UR - https://europepmc.org/article/MED/42868980
AB - 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.
SN - 2452-302X
ER -