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Review
. 2020 Dec 4:11:603187.
doi: 10.3389/fimmu.2020.603187. eCollection 2020.

The Roles of Inflammation in Keloid and Hypertrophic Scars

Zheng-Cai Wang  1 , Wan-Yi Zhao  1 , Yangyang Cao  2 , Yan-Qi Liu  1 , Qihang Sun  3 , Peng Shi  3 , Jia-Qin Cai  1 , Xiao Z Shen  2 , Wei-Qiang Tan  1
Affiliations
Review

The Roles of Inflammation in Keloid and Hypertrophic Scars

Zheng-Cai Wang et al. Front Immunol. .

Abstract

The underlying mechanisms of wound healing are complex but inflammation is one of the determining factors. Besides its traditional role in combating against infection upon injury, the characteristics and magnitude of inflammation have dramatic impacts on the pathogenesis of scar. Keloids and hypertrophic scars are pathological scars that result from aberrant wound healing. They are characterized by continuous local inflammation and excessive collagen deposition. In this review, we aim at discussing how dysregulated inflammation contributes to the pathogenesis of scar formation. Immune cells, soluble inflammatory mediators, and the related intracellular signal transduction pathways are our three subtopics encompassing the events occurring in inflammation associated with scar formation. In the end, we enumerate the current and potential medicines and therapeutics for suppressing inflammation and limiting progression to scar. Understanding the initiation, progression, and resolution of inflammation will provide insights into the mechanisms of scar formation and is useful for developing effective treatments.

Keywords: hypertrophic scar; immune cells; inflammatory mediators; keloid; potential therapeutics; signal transduction pathways.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
The roles of different inflammatory cells in aberrant scar formation. Red arrows, Positive effects; Green arrows, Negative effects; Treg, regulatory T cells; Th, Helper T cells; TGF-β, Transforming growth factor-β; PDGF-CC, Platelet-derived growth factor–CC; IFN-γ, Interferon γ; IL-4, interleukins-4; IL-13, interleukins-13; VEGF, Vascular endothelial growth factor; bFGF, basic fibroblast growth factor; NETs, Neutrophil extracellular traps.
Figure 2
Figure 2
The roles of inflammatory factors and inflammatory signaling pathways in aberrant scar formation. Red arrows, Positive effects; Green arrows, Negative effects; TLRs, Toll-Like Receptors; DAMPs, damage associated molecular patterns; NF-κB, Nuclear factor kappa B (NF-κB); STAT-3, Signal transducer and activator of transcription 3; FAK, Focal adhesion kinase; IL-6, Interleukin-6; IL-8, Interleukin-8; MCP-1, Monocyte chemoattractant protein-1; CXCL12, Chemokines ligand 12.
Figure 3
Figure 3
Current and potential treatments for pathological scar through suppressing inflammation. IL-6, Interleukin-6; TNF-α, tumor necrosis factor-α; TSG-6, tumor necrosis factor alpha stimulated gene-6; IL-1β, Interleukin-1β; DAMPs, damage associated molecular patterns; PLC ϵ, phospholipase ϵ.
See this image and copyright information in PMC

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