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Related Experiment Video

Updated: Jun 13, 2026

Isolation, Culture, and Characterization of Primary Dermal Fibroblasts from Human Keloid Tissue
04:41

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Published on: July 28, 2023

Integrated Transcriptomic Analysis Suggests a C1Q-Related Macrophage-Fibroblast Signaling Axis in Keloids.

Yutong Yuan1, Yuanbo Liu1, Ningbei Yin1

  • 1Plastic Surgery Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, No. 33 Ba-Da-Chu Road, Beijing 100144, China.

International Journal of Molecular Sciences
|June 12, 2026
PubMed
Summary
This summary is machine-generated.

This study identifies a potential communication pathway involving C1Q, linking macrophages to fibroblast activation in keloid scars. This sheds light on immune cells driving scar progression and suggests new therapeutic targets.

Keywords:
C1QLRP1bioinformatics analysiscell–cell communicationkeloidmacrophagesingle-cell transcriptomics

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Area of Science:

  • Dermatology
  • Immunology
  • Molecular Biology

Background:

  • Keloids are complex scars involving immune cells and fibroblasts.
  • The precise mechanisms of macrophage influence on fibroblast activation in keloids are unclear.

Purpose of the Study:

  • To investigate macrophage-fibroblast communication in the keloid microenvironment.
  • To identify molecular pathways driving fibroblast activation in keloids.

Main Methods:

  • Integrated bulk and single-cell RNA sequencing of keloid tissues.
  • Tissue immunofluorescence and in vitro cell culture experiments.
  • Assessed C1Q stimulation and RAP intervention in keloid fibroblasts.

Main Results:

  • Identified profibrotic fibroblast states and M2-like macrophages in keloids.
  • Nominated C1QB (macrophage ligand) and LRP1 (fibroblast receptor) as key interactors.
  • C1Q stimulation increased ACTA2 expression in keloid fibroblasts.

Conclusions:

  • Proposed a C1Q-mediated macrophage-fibroblast communication axis in keloid pathogenesis.
  • Provides a framework for understanding immune-driven scar progression.
  • Suggests potential targets for keloid intervention strategies.