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Burns Trauma. 2017 May 22;5:14. doi: 10.1186/s41038-017-0080-1. eCollection 2017.

Current progress in understanding the molecular pathogenesis of burn scar contracture.

Author information

1
Institute of Burn Research, State Key Laboratory of Trauma, Burns and Combined Injuries, Chongqing Key Laboratory for Disease Proteomics, Southwest Hospital, Third Military Medical University, Chongqing, 400038 China.
2
Department of Burns, First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080 China.

Abstract

Abnormal wound healing is likely to induce scar formation, leading to dysfunction, deformity, and psychological trauma in burn patients. Despite the advancement of medical care treatment, scar contracture in burn patients remains a challenge. Myofibroblasts play a key role in scar contracture. It has been demonstrated that myofibroblasts, as well as inflammatory cells, fibroblasts, endothelial cells, and epithelial cells, secrete transforming growth factor-β1 (TGF-β1) and other cytokines, which can promote persistent myofibroblast activation via a positive regulation loop. In addition to the cellular contribution, the microenvironments, including the mechanical tension and integrin family, are also involved in scar contracture. Most recently, eukaryotic initiation factor 6 (eIF6), an upstream regulator of TGF-β1, has been demonstrated to be involved in myofibroblast differentiation and contraction in both in vitro fibroblast-populated collagen lattice (FPCL) and in vivo external mechanical stretch models. Moreover, the data showed that P311 could induce the transdifferentiation of epidermal stem cells to myofibroblasts by upregulating TGF-β1 expression, which mediated myofibroblast contraction. In this review, we briefly described the most current progress on the biological function of myofibroblasts in scar contracture and subsequently summarized the molecular events that initiated contracture. This would help us better understand the molecular basis of scar contracture as well as to find a comprehensive strategy for preventing/managing scar contracture.

KEYWORDS:

Burn; Contracture; Molecular pathogenesis; Scar

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