Identification of Pathways That Drive Myofibroblast Transformation in Hypertrophic Scars

Article Open Access

Identification of Pathways That Drive Myofibroblast Transformation in Hypertrophic Scars

Author Information
1
Fibrosis Research Group, Medical Technology Research Centre, School of Allied Health and Social Care, Faculty of Health, Medicine & Social Care, Anglia Ruskin University, Chelmsford CM1 1SQ, UK
2
School of Medicine, Faculty of Health, Medicine & Social Care, Anglia Ruskin University, Chelmsford CM1 1SQ, UK
3
St. Andrew’s Centre for Plastic Surgery and Burns, Broomfield Hospital, Chelmsford CM1 7ET, UK
*
Authors to whom correspondence should be addressed.

Received: 28 August 2025 Accepted: 28 September 2025 Published: 09 October 2025

Creative Commons

© 2025 The authors. This is an open access article under the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).

Views:31
Downloads:7
Fibrosis 2025, 3(4), 10011; DOI: 10.70322/fibrosis.2025.10011
ABSTRACT: Hypertrophic scars (HTS) are a common complication of burn injuries and are characterized by excessive dermal fibrosis driven by the transformation of resident dermal fibroblasts to profibrotic myofibroblasts. Although single cell and bulk RNA transcriptomics analysis of HTS and normal skin tissue samples were performed previously, transcriptomics of the transformation of fibroblasts to myofibroblasts has not been studied. Here, we report the data obtained from RNA sequencing of fibroblasts before and after exposure to transforming growth factor beta 1 (TGF-β1) and highlight the pathways that are up- and down-regulated during myofibroblast transformation. Our results suggest increased cellular signalling and rewiring, proliferative surge, immune-like and metabolic reprogramming, and delayed structural remodelling as four groups of events during the transformation of human primary dermal fibroblasts to myofibroblasts.
Keywords: Fibrosis; Hypertrophic scar; Fibroblast; Myofibroblast; Transforming growth factor beta 1; Skin; Burns

Graphical Abstract

TOP