A Review of Hypertrophic Scar and Keloid Treatment and Prevention in the Pediatric Population: Where Are We Now?

Menchaca, Alicia D; Style, Candace C.; Olutoye, Oluyinka O.

doi:10.1089/wound.2021.0028

Cited by 10 publications

(3 citation statements)

References 92 publications

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“…Hence, it is crucial to explore more effective treatment approaches. 1 , 8 In recent years, an increasing number of studies have identified drugs derived from traditional Chinese medicine. These drugs have demonstrated definite therapeutic effects and fewer side effects, thereby offering a broader range of scar treatment options.…”

Section: Discussionmentioning

confidence: 99%

Exploring the Potential of Hesperidin in Preventing Hypertrophic Scars: Insights from a Rabbit Ear Model

Yang,

Zhong,

Zhao

et al. 2023

CCID

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Background Hypertrophic scars, commonly occurring after trauma or surgery in critical areas like the head and joints, pose significant challenges to both physical and mental health due to their impact on skin function and aesthetics. While the complex pathogenesis involves fibroblast activation and collagen deposition, effective treatments are lacking, underscoring the importance of exploring pathogenesis and targeted therapies. Hesperidin, a bioactive compound in citrus fruits with diverse health benefits, including anti-fibrotic and anti-angiogenic effects, is the focus of this study with the aim of investigating its impact on hypertrophic scar formation, given its potential to promote blood flow and improve skin microcirculation. Objective This study aimed to observe the inhibitory effect of topical hesperidin on hypertrophic scars in rabbits. Methods A total of 8 healthy adult New Zealand white rabbits were used to establish a rabbit hypertrophic scarring animal model. Five wounds were created on each rabbit’s two ears, with three wounds on the left ear (groups A, B, and C) and two wounds on the right ear (groups D and E). After six days of wound drying postoperatively, the wounds were locally treated with medication as followed: group A, 0.1% hesperidin; group B, 1% hesperidin; group C, 1% triamcinolone acetonide; group D, Vaseline; and group E, blank control without any medication. After 28 days, the scar tissue samples were collected for histological examination. Results The results showed that the scar texture of groups B and C was softer and lighter in color, and the number of fibroblasts, capillaries, and inflammatory cells in the tissue was significantly less than those in the other three groups. The hypertrophic scar indices of groups B and C were significantly smaller than those of groups A, D, and E, and the difference was statistically significant (P < 0.05). There were no significant difference between groups B and C. Conclusion Topical application of hesperidin demonstrated promising potential for reducing hypertrophic scar formation in rabbits.

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Section: Discussionmentioning

confidence: 99%

Exploring the Potential of Hesperidin in Preventing Hypertrophic Scars: Insights from a Rabbit Ear Model

Yang,

Zhong,

Zhao

et al. 2023

CCID

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“…The current treatment for keloids includes traditional surgical excision, cryotherapy, cryotherapy in combination with other methods such as intralesional steroid injection, external beam therapy, brachytherapy, and laser therapy [ 26 – 28 ]. Keloid tissue is characterized by excessive accumulation of extracellular matrix collagen in the dermis and subcutaneous tissue.…”

Section: Discussionmentioning

confidence: 99%

RUNX3 mediates keloid fibroblast proliferation through deacetylation of EZH2 by SIRT1

Liu

Yan

et al. 2022

BMC Mol and Cell Biol

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Background Keloid is a benign proliferative fibrous disease featured by excessive fibroblast proliferation after skin injury. However, the mechanism of abnormal cell proliferation is still unclear. Herein, we investigated the mechanism of abnormal proliferation in keloids involving Sirtuin 1(SIRT1)/ Zeste Homolog 2 (EZH2)/ Runt-related transcription factor 3 (RUNX3). Methods HE staining was used to observe the histopathological changes. Western blot was performed to detect SIRT1/EZH2/RUNX3 and cell cycle related proteins. RT-PCR detected EZH2 mRNA. After knockdown of EZH2 or overexpression of RUNX3, cell proliferation and cell cycle was analyzed. Immunoprecipitation was used to detect acetylated EZH2. Results The results showed that overexpression of RUNX3 inhibited cell proliferation and arrested cell cycle at G1/S phase, whereas inhibition of SIRT1 promoted cell proliferation and G1/S phase of the cell cycle. Knockdown of EZH2 promoted the expression of RUNX3, inhibited cell proliferation and shortened the progression of G1 to S phase. Simultaneous knockdown of EZH2 and inhibition of SIRT1 reversed these effects. Inhibition of SIRT1 increased its protein stability by increasing EZH2 acetylation, thereby reducing the expression of RUNX3 and promoting cell proliferation. Conclusions Conclusively, the SIRT1/EZH2/RUNX3 axis may be an important pathway in the regulation of abnormal proliferation in keloids.

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“…Skin is the first line of defense from external factors, and there are many destructive external stimuli that can lead to hypertrophic scar (HS), such as surgery, piercings, acne, tattooing, burns, lacerations, abrasions, vaccinations, and even insect bites [1] . HS formation occurs as a result of skin injury, which leads to esthetic destruction and functional impairment, resulting in physiological and psychological problems [ 2 , 3 ].…”

Section: Introductionmentioning

confidence: 99%

HSFAS mediates fibroblast proliferation, migration, trans-differentiation and apoptosis in hypertrophic scars via interacting with ADAMTS8

Ma,

Liu,

Xia

et al. 2023

ABBS

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Hypertrophic scar (HS) is one of the most common sequelae of patients, especially after burns and trauma. The roles of regulatory long noncoding RNAs (lncRNAs) in mediating HS remain underexplored. Human hypertrophic scar-derived fibroblasts (HSFBs) have been shown to exert more potent promoting effects on extracellular matrix (ECM) accumulation than normal skin-derived fibroblasts (NSFBs) and are associated with enhanced HS formation. The purpose of this study is to search for lncRNAs enriched in HSFBs and investigate their roles and mechanisms. LncRNA MSTRG.59347.16 is one of the most highly expressed lncRNAs in HS detected by lncRNA-seq and qRT-PCR and named as hypertrophic scar fibroblast-associated lncRNA (HSFAS). HSFAS overexpression significantly induces fibroblast proliferation, migration, and myofibroblast trans-differentiation and inhibits apoptosis in HSFBs, while knockdown of HSFAS results in augmented apoptosis and attenuated proliferation, migration, and myofibroblast trans-differentiation of HSFBs. Mechanistically, HSFAS suppresses the expression of A disintegrin and metalloproteinase with thrombospondin motifs 8 (ADAMTS8). ADAMTS8 knockdown rescues downregulated HSFAS-mediated fibroblast proliferation, migration, myofibroblast trans-differentiation and apoptosis. Thus, our findings uncover a previously unknown lncRNA-dependent regulatory pathway for fibroblast function. Targeted intervention in the HSFAS-ADAMTS8 pathway is a potential therapy for HS.

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A Review of Hypertrophic Scar and Keloid Treatment and Prevention in the Pediatric Population: Where Are We Now?

Cited by 10 publications

References 92 publications

Exploring the Potential of Hesperidin in Preventing Hypertrophic Scars: Insights from a Rabbit Ear Model

Exploring the Potential of Hesperidin in Preventing Hypertrophic Scars: Insights from a Rabbit Ear Model

RUNX3 mediates keloid fibroblast proliferation through deacetylation of EZH2 by SIRT1

HSFAS mediates fibroblast proliferation, migration, trans-differentiation and apoptosis in hypertrophic scars via interacting with ADAMTS8

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