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Related Experiment Video

Updated: Sep 14, 2025

Author Spotlight: The Significance of Isolation, Culture, and Adipogenic Induction of SVF-Derived Preadipocytes from Mouse Perivascular Adipose Tissue
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Circulating adiponectin levels in systemic sclerosis: A meta-analysis and bidirectional Mendelian randomization

Tahzeeb Fatima1, Cecilia Överdahl1,2, Cristina Maglio1,2

  • 1Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.

Journal of Scleroderma and Related Disorders
|July 21, 2025
PubMed
Summary

This study found lower adiponectin levels in systemic sclerosis patients. Mendelian randomization revealed a causal link where systemic sclerosis liability lowers adiponectin, not the reverse.

Keywords:
Mendelian randomizationSystemic sclerosisadiponectindiffuse cutaneouslimited cutaneousmeta-analysis

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Area of Science:

  • Endocrinology
  • Rheumatology
  • Genetics

Background:

  • Previous research on adiponectin and systemic sclerosis (SSc) lacks consistent findings and a clear causal relationship.
  • Adiponectin, a key adipokine, plays roles in inflammation and metabolism, potentially influencing SSc pathogenesis.
  • Understanding this relationship is crucial for developing targeted therapies for SSc.

Purpose of the Study:

  • To conduct an updated meta-analysis to assess the association between circulating adiponectin and SSc.
  • To investigate a potential causal relationship between adiponectin levels and SSc risk using Mendelian randomization.

Main Methods:

  • A systematic literature search was performed across PubMed, Embase, and Web of Science up to September 2024.
  • Meta-analysis pooled data from observational studies, calculating standardized mean differences.
  • Bidirectional Mendelian randomization utilized genome-wide association study summary statistics to infer causality.

Main Results:

  • Meta-analysis of 7 studies (439 SSc cases) showed reduced adiponectin in SSc patients (SMD = -0.16, p=0.07), significant in diffuse cutaneous SSc (p=0.003) but not limited cutaneous SSc (p=0.81).
  • Forward Mendelian randomization found no causal effect of adiponectin on SSc risk (OR = 1.21, p=0.57).
  • Reverse Mendelian randomization indicated a causal effect of genetic liability to SSc on lowering adiponectin levels (β = -0.027, p=6.8E-06).

Conclusions:

  • Observational data confirm lower adiponectin levels in systemic sclerosis patients.
  • Mendelian randomization established a causal link: genetic predisposition to SSc leads to reduced adiponectin.
  • Further research in diverse populations is needed to explore these findings beyond European ancestry.