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Related Experiment Video

Updated: Jul 10, 2026

Visualizing Scar Development Using SCAD Assay - An Ex-situ Skin Scarring Assay
07:40

Visualizing Scar Development Using SCAD Assay - An Ex-situ Skin Scarring Assay

Published on: April 28, 2022

FOSL1-mediated super-enhancer facilitates pathological scarring.

Yixin Sun1, Zhizhuo Chen2, Mengdi Zhang3

  • 1Department of Plastic and Aesthetic Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China; Center for Plastic & Reconstructive Surgery, Department of Plastic & Reconstructive Surgery, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou 310014, Zhejiang, China; Center for Regenerative Medicine & Plastic Surgery Research, Peking Union Medical College Hospital, Beijing 100005, China.

Cell Reports
|July 8, 2026
PubMed
Summary
This summary is machine-generated.

Researchers identified FOSL1+ keratinocytes driving scar formation by secreting MMP3. Inhibiting FOSL1 reduced scar size in models, suggesting a new therapeutic target for pathological scarring.

Keywords:
CP: stem cell researchcellular crosstalkfibroblastskeratinocytespathological scarwound healing

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Area of Science:

  • Dermatology
  • Molecular Biology
  • Wound Healing Research

Background:

  • Pathological scarring, marked by excessive fibrosis, results from abnormal wound healing.
  • The molecular drivers of scar formation are not fully understood.
  • Identifying these drivers is crucial for developing effective treatments.

Purpose of the Study:

  • To identify molecular factors contributing to hypertrophic scars and keloids.
  • To elucidate the mechanism by which these factors promote fibrosis.
  • To evaluate a potential therapeutic intervention targeting these factors.

Main Methods:

  • Single-cell RNA sequencing (scRNA-seq) was employed to analyze cell populations in scar tissue.
  • Investigated the role of FOSL1 (a transcription factor) and MMP3 (a matrix metalloproteinase) in fibrosis.
  • Utilized in vivo xenogenic keloid models to test a FOSL1 inhibitor (SR11302).

Main Results:

  • Identified FOSL1-expressing keratinocytes that are expanded in hypertrophic scars and keloids.
  • These FOSL1+ keratinocytes exhibit epithelial-mesenchymal transition (EMT) and secrete MMP3, activating fibroblasts.
  • FOSL1 directly upregulates MMP3 transcription via a MED-1 super-enhancer, promoting inflammation and fibrosis.
  • SR11302 treatment significantly reduced scar formation in preclinical models.

Conclusions:

  • Aberrant FOSL1+ keratinocytes and their MMP3 secretion are key drivers of pathological scarring.
  • Targeting FOSL1 represents a promising therapeutic strategy for managing excessive fibrosis and improving wound healing.
  • This research provides a foundation for developing interventions aimed at achieving scarless healing.