Association of interleukin-6 gene polymorphisms and circulating levels with keloid scars in a Chinese Han population

Zhu, Xiaoqin; Li, W.Z.; Li, H.; Fu, Chunli; Liu, J.

doi:10.4238/gmr16029110

Cited by 15 publications

(12 citation statements)

References 23 publications

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“…In line with the findings of studies included in our systematic review, 28–31 Xue et al also demonstrated elevated IL‐6 levels in KFs 35 . Additionally, the IL‐6‐572 GG genotype was associated with an increased risk for keloids in an Egyptian, South‐Eastern Chinese and Japanese population 36–38 . Moreover, IL‐6 was significantly decreased in early foetal fibroblasts, possibly contributing to scarless healing 39,40 .…”

Section: Discussionsupporting

confidence: 86%

“…35 Additionally, the IL-6-572 GG genotype was associated with an increased risk for keloids in an Egyptian, South-Eastern Chinese and Japanese population. [36][37][38] Moreover, IL-6 was significantly decreased in early foetal fibroblasts, possibly contributing to scarless healing. 39,40 Interestingly, the corticosteroid triamcinolone, which is a first-line treatment of keloids, decreases IL-6 induced angiogenesis.…”

Section: Interleukins and Jak-stat Pathwaymentioning

confidence: 99%

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The JAK–STAT pathway in keloid pathogenesis: a systematic review with qualitative synthesis

Yin

Wolkerstorfer

Lapid

et al. 2023

Experimental Dermatology

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Keloid tissues contain inflammatory cells and upregulated pro‐inflammatory cytokines. The Janus kinase (JAK)‐signal transducer and activator of transcription (STAT) pathway mediate cellular responses to these cytokines. We performed a systematic review on the role of the JAK–STAT pathway in keloid pathogenesis and the evidence for JAK–STAT inhibitors in keloid treatment. The search combined the terms (1) keloid and (2) JAK or TYK or STAT and included MeSH terms and synonyms. Two reviewers screened the articles and assessed the full texts on eligibility. Data were collected on the tested drugs and molecules, the type of cells and tissues used in the experiments, and study findings on the association between the JAK–STAT pathway and keloid cells and tissues. A total of twenty preclinical studies were included. Eleven preclinical studies proved that STAT3 expression and phosphorylation are enhanced in keloid tissue and keloid fibroblasts. Thirteen different JAK and/or STAT inhibitors were investigated. Tested drugs inhibited keloid progression as demonstrated by different processes, including reduced collagen production, cell proliferation and migration, increased cell cycle arrest and apoptosis, enhanced antioxidant responses, decreased (paracrine) signalling, and decreased profibrotic gene expression. No clinical studies have been published to date. Preclinical studies indicate a role for the JAK–STAT pathway in keloid pathogenesis and a potential role for JAK–STAT inhibitors in keloid treatment. The effect of these drugs should be further investigated on relevant biomarkers in a human keloid skin model, preferably including immune cells besides keloid fibroblasts and keratinocytes and in clinical studies.

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Section: Discussionsupporting

confidence: 86%

Section: Interleukins and Jak-stat Pathwaymentioning

confidence: 99%

The JAK–STAT pathway in keloid pathogenesis: a systematic review with qualitative synthesis

Yin

Wolkerstorfer

Lapid

et al. 2023

Experimental Dermatology

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“…When combining TA with IFN‐γ STAT3 inhibition and STAT1 induction may occur in parallel. In recent years is has been discussed whether IL‐6 overexpression as well as genetic analysis concerning IL‐6 polymorphisms can be used as potential prognostic tools to evaluate the risk of keloid development ; therefore it seems to be possible that counter regulating IL‐6 overexpression might be a critical trigger to inhibit the prolonged inflammatory phase of wound healing in keloids. Even though the relative TA‐dependent IL‐6 reduction was less pronounced in keloid fibroblasts than in normal fibroblasts it has to be considered that in clinical settings cytokine secretion of normal cells may also trigger paracrine response of the keloid cells by reducing the total cytokine concentration in the area surrounding the keloid.…”

Section: Discussionmentioning

confidence: 99%

Normal and keloid fibroblasts are differentially influenced by IFN‐γ and triamcinolone as well as by their combination

Euler

Valesky

Meißner

et al. 2019

Wound Repair Regeneration

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Impaired wound healing as well as imbalanced cell proliferation and extracellular matrix synthesis and degeneration can cause aberrant scarring. The most severe impacts of such scarring on patients' lives are stigmatization and physical restriction. Although, a broad variety of combinatorial approaches with, e.g., glucocorticoids, chemotherapeutics, and immunomodulators are used, there is still a high recurrence rate of keloids. The aim of this study was to investigate which influence interferon γ (IFN-γ, 1.000-10.000 IU/mL) and/or triamcinolone acetonide (TA, 1 μg/mL) have on proliferation, cell viability, collagen type I synthesis, and cytokine secretion in healthy and keloid fibroblasts. It was shown that mono-treatment with IFN-γ or TA for 2 days induced a severe reduction of the proliferative potential in both cell species. The combinatory treatment (IFN-γ plus TA) of keloid fibroblasts enhanced the anti-proliferative effect of the mono-treatments, whereas no additional anti-proliferative effect was observed in normal fibroblasts. Furthermore, we observed that the combinatory treatment regimen reduced the expression of α-smooth muscle actin (α-SMA), an actin isotype contributing to cell-generated mechanical tension, in keloid fibroblasts. In normal fibroblasts, α-SMA was reduced by the mono-treatment with IFN-γ as well as by the combinatory treatment. The analysis of collagen-type I synthesis revealed that TA did not reduce collagen type I synthesis in normal fibroblasts but in keloid fibroblasts. IFN-γ reduced in both cell species the collagen type I synthesis. The combination of TA and IFN-γ intensified the previously observed collagen type I synthesis reduction in keloid fibroblasts. The herein presented data suggest the combinatory application of IFN-γ and TA as a promising therapy concept for keloids.

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“…Keloids are associated with IL-6 gene polymorphisms in Japanese and Chinese populations. [23][24] Furthermore, BM-MSCs reduce the level of IL-6 in a liver fibrosis model, suggesting that they may play the same role in keloids. [25][26][27]…”

Section: Inhibition Of Inflammatory Cell Infiltrationmentioning

confidence: 99%

Possible Mechanisms and Prospects of Stem Cell Therapy for Keloids

Chen

2019

Int J Dermatol Venereol

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Association of interleukin-6 gene polymorphisms and circulating levels with keloid scars in a Chinese Han population

Cited by 15 publications

References 23 publications

The JAK–STAT pathway in keloid pathogenesis: a systematic review with qualitative synthesis

The JAK–STAT pathway in keloid pathogenesis: a systematic review with qualitative synthesis

Normal and keloid fibroblasts are differentially influenced by IFN‐γ and triamcinolone as well as by their combination

Possible Mechanisms and Prospects of Stem Cell Therapy for Keloids

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