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Review
. 2016 Jan 21:4:2.
doi: 10.1186/s41038-015-0026-4. eCollection 2016.

The molecular basis of hypertrophic scars

Zhensen Zhu  1 , Jie Ding  2 , Edward E Tredget  3
Affiliations
Review

The molecular basis of hypertrophic scars

Zhensen Zhu et al. Burns Trauma. .

Abstract

Hypertrophic scars (HTS) are caused by dermal injuries such as trauma and burns to the deep dermis, which are red, raised, itchy and painful. They can cause cosmetic disfigurement or contractures if craniofacial areas or mobile region of the skin are affected. Abnormal wound healing with more extracellular matrix deposition than degradation will result in HTS formation. This review will introduce the physiology of wound healing, dermal HTS formation, treatment and difference with keloids in the skin, and it also review the current advance of molecular basis of HTS including the involvement of cytokines, growth factors, and macrophages via chemokine pathway, to bring insights for future prevention and treatment of HTS.

Keywords: Animal model; Cytokines; Growth factors; Hypertrophic scars; Macrophages; Stromal cell-derived factor 1/CXCR4 signaling.

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Figures

Fig. 1
Fig. 1
Patients with HTS. A 24 year-old white man, 11 months after a 21 % TBSA burn. This patient developed HTS, resulting in cosmetic and functional problems that included restricted opening of mouth and tight web spaces of fingers that limited range of motion on hands (From Tredget EE, Levi B, Donelan MB. Biology and principles of scar management and burn reconstruction. Surg Clin North Am. 2014 Aug;94(4):793–815. With permission)
Fig. 2
Fig. 2
The roles of monocytes and polarized macrophages in HTS formation. We hypothesize that monocytes in the blood are recruited to the injured site via the SDF-1/CXCR4 signaling pathway and differentiate into polarized macrophages. The polarized M1 and M2 macrophages then exert their functions via various signaling pathways and involve in wound healing and HTS formation
See this image and copyright information in PMC

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