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Triglycerides and T Cells in Cardiovascular Risk: Inflammatory Transcriptomic Profile in Hypertriglyceridemia

Nathalie A Reilly1, Janneke W C M Mulder2, Koen F Dekkers3

  • 1Molecular Epidemiology, Department of Biomedical Data Sciences, Leiden University Medical Center, Leiden, the Netherlands; Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands.

JACC. Basic to Translational Science
|August 22, 2025
PubMed
Summary
This summary is machine-generated.

Elevated triglycerides may promote cardiovascular disease (CVD) by altering T cell gene expression. Primary moderate hypertriglyceridemia showed a proinflammatory T cell profile, linked to increased CVD risk.

Keywords:
T cellsatherosclerosishypertriglyceridemiahypotriglyceridemiatranscriptomicstriglycerides

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Area of Science:

  • Immunology
  • Cardiovascular Science
  • Genomics

Background:

  • Atherosclerosis, a major cause of cardiovascular disease (CVD), involves triglycerides and T cells.
  • Moderately elevated triglycerides are a recognized causal risk factor for CVD.
  • T cells are integral components of atherosclerotic plaques.

Purpose of the Study:

  • To investigate transcriptomic differences in T cells across various triglyceride levels.
  • To understand the molecular mechanisms linking triglyceride levels to T cell function and CVD risk.

Main Methods:

  • Cross-sectional study analyzing RNA sequencing data from CD4+ and CD8+ T cells.
  • Participants included individuals with primary/secondary moderate hypertriglyceridemia, severe hypertriglyceridemia, and hypotriglyceridemia.
  • Transcriptomic profiles were compared based on triglyceride status.

Main Results:

  • Primary moderate hypertriglyceridemia revealed a proinflammatory T cell transcriptomic profile, notably increased interleukin-6 receptor (IL6R) expression.
  • Similar proinflammatory patterns were observed in CD8+ T cells and, to a lesser extent, in secondary moderate hypertriglyceridemia.
  • Hypotriglyceridemia showed reversed transcriptomic differences, while severe hypertriglyceridemia showed no significant changes.

Conclusions:

  • Elevated triglycerides, particularly in primary moderate hypertriglyceridemia, may drive CVD by inducing a proinflammatory T cell phenotype.
  • The findings highlight a potential molecular link between triglyceride levels, T cell transcriptomics, and atherosclerosis pathogenesis.
  • Targeting triglyceride-mediated T cell inflammation could offer novel therapeutic strategies for CVD prevention.