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Related Experiment Video

Updated: Jan 29, 2026

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Polygenic Risk and Linked Metabolic Profile in Systemic Lupus Erythematosus: Cross-Sectional Insights.

Andrea Higuera-Gómez1,2, María Martínez-Urbistondo3, Amanda Cuevas-Sierra2,4

  • 1Department of Pharmacy and Nutrition, Faculty of Biomedical and Health Sciences, Universidad Europea de Madrid, Calle Tajo s/n, Villaviciosa de Odón, 28670 Madrid, Spain.

Genes
|January 28, 2026
PubMed
Summary

Genetic predisposition influences metabolic variations in systemic lupus erythematosus (SLE) patients, but not inflammatory markers. Understanding this interplay is key for personalized SLE management and cardiovascular risk assessment.

Keywords:
autoimmune diseasescardiovascular riskgenetic predispositioninflammationpolygenic risk score (PRS)precision medicinesystemic lupus erythematosus (SLE)

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Area of Science:

  • Immunology
  • Genetics
  • Metabolic Diseases

Background:

  • Systemic lupus erythematosus (SLE) is a complex autoimmune disease with multifactorial origins.
  • Genetic predisposition, quantified by polygenic risk scores (PRS), plays a role in SLE.
  • The relationship between genetic susceptibility and metabolic dysfunction in SLE is not well understood.

Purpose of the Study:

  • To investigate associations between SLE-related PRS and metabolic, inflammatory, and clinical parameters.
  • To explore the interplay between genetic predisposition and metabolic dysfunction in SLE patients.

Main Methods:

  • Ninety-three participants (56 SLE patients, 37 metabolic syndrome controls) were analyzed.
  • Polygenic risk scores (PRS) were calculated using validated lupus-associated single nucleotide variants (SNVs).

Main Results:

  • SLE patients exhibited a distinct metabolic profile compared to controls, with lower BMI, visceral fat, blood pressure, glucose, and liver enzymes.
  • In SLE patients, PRS correlated with specific clinical and biochemical features.
  • PRS showed an inverse association with ferritin levels; other markers were influenced by clinical factors.

Conclusions:

  • Polygenic predisposition contributes to metabolic phenotype variability in SLE but does not independently drive inflammation.
  • SLE patients present metabolic and inflammatory alterations linked to cardiovascular risk.
  • Integrating PRS with metabolic profiling can enhance personalized SLE management and cardiovascular risk evaluation.