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Updated: Jul 13, 2026
04:41
Isolation, Culture, and Characterization of Primary Dermal Fibroblasts from Human Keloid Tissue
Published on: July 28, 2023
Transforming growth factor beta (TGFbeta) and keloid disease
Jagajeevan Jagadeesan1, Ardeshir Bayat
1Department of Plastic and Reconstructive Surgery, Royal Preston Hospital, Sharoe Green Lane, Fulwood, Preston PR2 9HT, UK.
International Journal of Surgery (London, England)
|July 31, 2007
Summary
Keloids, a wound healing disorder, may involve Transforming Growth Factor beta (TGFbeta). This review explores TGFbeta
Area of Science:
- Dermatology and Molecular Biology
Background:
- Keloids are benign fibroproliferative diseases resulting from abnormal wound healing.
- Transforming Growth Factor beta (TGFbeta) family members are implicated in keloid pathogenesis.
- TGFbeta is also linked to fibrotic conditions in organs like the liver, kidney, and lungs.
Purpose of the Study:
- To review the morphology and mechanism of action of TGFbeta and its isoforms.
- To present current literature on the role of TGFbeta isoforms, receptors, and SMAD signaling in keloid disease.
- To highlight the potential for developing novel keloid therapeutics based on TGFbeta pathways.
Main Methods:
- Literature review of scientific articles on keloid disease and TGFbeta signaling.
- Analysis of the role of TGFbeta isoforms, their receptors, and intracellular pathways (SMAD).
Main Results:
- TGFbeta family members play a significant role in keloid pathogenesis.
- Specific TGFbeta isoforms, receptors, and the SMAD pathway are key in keloid development.
- Understanding these mechanisms is crucial for therapeutic development.
Conclusions:
- TGFbeta signaling is a critical factor in keloid formation.
- Targeting TGFbeta pathways offers potential for new keloid treatments.
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