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Updated: Dec 23, 2025

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

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

Published on: July 28, 2023

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Nintedanib inhibits keloid fibroblast functions by blocking the phosphorylation of multiple kinases and enhancing

Bo-Ya Zhou1, Wen-Bo Wang1, Xiao-Li Wu1

  • 1Department of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Tissue Engineering Research, Shanghai, 200011, China.

Acta Pharmacologica Sinica
|April 25, 2020
PubMed

Insights

Nintedanib, a tyrosine kinase inhibitor, effectively suppressed keloid fibroblast proliferation, migration, and collagen production in vitro and ex vivo. This study suggests nintedanib as a promising targeted therapy for keloid systemic treatment.

Area of Science:

  • Dermatology
  • Oncology
  • Pharmacology

Background:

  • Keloids are benign skin tumors marked by excessive cell growth, invasion, and high recurrence rates.
  • Nintedanib is a multi-target receptor tyrosine kinase inhibitor with anti-cancer and anti-angiogenic properties.

Purpose of the Study:

  • To investigate the efficacy of nintedanib in treating keloid fibroblasts.
  • To evaluate nintedanib's effects on keloid cell proliferation, migration, invasion, and extracellular matrix production.

Main Methods:

  • Keloid fibroblasts from 54 scar samples were treated with nintedanib (1-4 μM) in vitro.
  • Gene and protein expression of key fibrotic factors were analyzed.
  • Ex vivo keloid tissue explants were used to assess drug effects on microvessel structure and cell behavior.

Main Results:

  • Nintedanib dose-dependently inhibited keloid fibroblast proliferation, cell cycle progression, migration, and invasion.
  • The drug significantly reduced the expression of collagen I, collagen III, fibronectin, and CTGF.
  • Nintedanib suppressed key signaling pathways (p38, JNK, ERK, STAT3, Smad) and disrupted microvessel structures ex vivo.

Conclusions:

  • Nintedanib demonstrates significant anti-keloid activity by targeting multiple pathways involved in keloid pathogenesis.
  • These findings support nintedanib as a potential novel systemic therapy for keloid scars.
Keywords:
MAPK signalingTGF-β/Smad signalinganti-keloid activityex vivo tissue explant modelkeloid fibroblastsnintedanib

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