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Updated: Jun 28, 2026

Multiplexed Analysis of Retinal Gene Expression and Chromatin Accessibility Using scRNA-Seq and scATAC-Seq
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Integrating Single-Cell Transcriptomics and Mendelian Randomization to Identify RAC1 as a Causal Metabolic Driver of

Xiaoqing Wang1, Zheng Zhang1, Enze Jiang2

  • 1Department of Dermatology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China, shsmu.edu.cn.

Mediators of Inflammation
|June 16, 2026
PubMed
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This summary is machine-generated.

Systemic sclerosis (SSc) involves pericyte dysfunction. This study identifies RAC1 as a causal factor, showing it drives progenitor-like pericyte activation and promotes fibrosis through metabolic changes and inflammation.

Area of Science:

  • Immunology
  • Genetics
  • Cell Biology

Background:

  • Systemic sclerosis (SSc) is an autoimmune disease causing vascular damage and fibrosis.
  • Pericyte dysfunction is implicated, but their heterogeneity and genetic drivers in SSc remain unclear.

Purpose of the Study:

  • To investigate the cellular and genetic basis of pericyte dysfunction in SSc.
  • To identify genetic mechanisms driving pathological pericyte transition.

Main Methods:

  • Integrated single-cell RNA sequencing (scRNA-seq) with genome-wide association study (GWAS) data.
  • Utilized bidirectional Mendelian randomization (MR) analysis, pseudotime trajectory, and cell-cell communication analysis.
  • Validated findings using external bulk RNA-seq datasets.

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Main Results:

  • Identified progenitor-like pericytes at the root of fibrotic differentiation.
  • RAC1 was a significant causal risk factor for SSc.
  • RAC1-positive pericytes showed increased pro-inflammatory crosstalk with macrophages and altered metabolism (riboflavin/thiamine).

Conclusions:

  • Established a mechanistic link between RAC1, progenitor-like pericyte activation, and SSc pathogenesis.
  • RAC1 drives pathological pericyte transition, metabolic reprogramming, and immune recruitment, creating a pro-inflammatory environment.
  • RAC1 presents a novel therapeutic target for SSc.