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Multi-Omics Evidence Linking Depression to MASLD Risk via Inflammatory Immune Signaling.

Keye Lin1, Yiwei Liu2, Xitong Liang1

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|January 28, 2026
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Summary
This summary is machine-generated.

Depression increases the risk of Metabolic Dysfunction-Associated Steatotic Fatty Liver Disease (MASLD), particularly in women, mediated by inflammation. The CD40LG-CD40 immune axis may be a key mechanism linking these conditions.

Keywords:
CD40LGMASLDdepressionimmune signalinginflammationsex differences

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Area of Science:

  • Integrative omics
  • Immunology
  • Metabolic disease research

Background:

  • Depression and Metabolic Dysfunction-Associated Steatotic Fatty Liver Disease (MASLD) are prevalent chronic conditions with unclear links.
  • Existing research lacks understanding of the causal relationship and underlying molecular mechanisms between depression and MASLD.

Purpose of the Study:

  • To investigate the causal role of depression in MASLD risk.
  • To explore the mediating effect of inflammation and immune signaling in this relationship.
  • To identify molecular pathways, including specific genes and cellular interactions, connecting depression and MASLD.

Main Methods:

  • Multi-level data integration: NHANES epidemiology, GWAS genetics, GEO transcriptomics, and single-cell RNA sequencing.
  • Cross-sectional epidemiological analysis and two-sample Mendelian randomization to establish causality and mediation.
  • Weighted gene co-expression network analysis and machine learning to identify hub genes.
  • Single-cell RNA sequencing to analyze gene expression dynamics at cellular resolution.

Main Results:

  • Depression significantly elevates MASLD risk (OR=1.39), especially in women, with inflammation markers (hs-CRP, GGT, ALP) acting as mediators.
  • Mendelian randomization confirmed a unidirectional causal effect from depression to MASLD (β=0.483).
  • The CD40LG-CD40 axis was identified as a molecular bridge, with CD40LG expression increasing in CD4+ T cells and CD40 in B cells during MASLD progression, notably in females.

Conclusions:

  • Converging multi-omics evidence supports a causal role for depression in MASLD development via inflammation-mediated immune signaling.
  • The CD40LG-CD40 axis represents a novel immune mechanism linking depression to MASLD pathogenesis.
  • This pathway offers potential therapeutic targets for gender-specific interventions in metabolic liver disease.