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Related Experiment Video

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Imaging Features of Systemic Sclerosis-Associated Interstitial Lung Disease
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Skin Transcriptomics Reveal Shared Molecular Mechanisms for Skin and Lung Involvement in Systemic Sclerosis.

Jana Zielonka1, Ningshan Li2, Yunqing Liu2

  • 1Pulmonary, Critical Care, and Sleep Medicine Section, Yale University, New Haven, Connecticut.

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|April 3, 2026
PubMed
Summary

A severe skin gene signature in systemic sclerosis (SSc) is linked to multiorgan damage, including lung impairment. This finding highlights shared fibrotic mechanisms and potential therapeutic targets in SSc-related interstitial lung disease (SSc-ILD).

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Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice
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Area of Science:

  • Immunology
  • Genomics
  • Pulmonology

Background:

  • Systemic sclerosis (SSc) involves immune dysregulation, vascular damage, and fibrosis.
  • SSc-related interstitial lung disease (SSc-ILD) is a major cause of mortality.
  • Biomarkers for SSc-ILD are crucial for understanding disease progression.

Purpose of the Study:

  • To investigate if skin gene expression (transcriptome) can reveal mechanisms of lung impairment in SSc-ILD.
  • To identify potential biomarkers associated with SSc-ILD severity.

Main Methods:

  • Multi-stage analysis of SSc skin transcriptomes.
  • Weighted gene correlation, gene set enrichment, and single-cell RNA sequencing.
  • Deconvolution of gene signatures in SSc skin and lung tissues.

Main Results:

  • Identified seven gene modules linked to skin and lung involvement.
  • Classified SSc patients into two groups: one with severe multiorgan involvement (increased skin fibrosis, decreased lung function).
  • Found enrichment of the KRAS pathway in severe SSc, particularly in stromal cells, and identified a severe cutaneous signature associated with multiorgan involvement.

Conclusions:

  • A severe cutaneous transcriptomic signature in SSc correlates with multiorgan involvement.
  • The KRAS pathway and specific cell types (stromal, immune) are implicated in SSc pathogenesis.
  • This signature offers a framework for understanding shared skin and lung fibrotic mechanisms in SSc.