Update on Keloid Management: Clinical and Basic Science Advances

Viera, Martha H.; Vivas, Alejandra C.; Berman, Brian

doi:10.1089/wound.2011.0313

Cited by 35 publications

(42 citation statements)

References 29 publications

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“…Keloids are abnormal scars that expand beyond the borders of the original wound and are a result of an aberrant wound healing process . These hyperfibrotic lesions, which are mostly prevalent in individuals of African descent, cause negative physical and psychological impact on patients . Although the exact aetiology of keloid formation in predisposed individuals is not completely understood, they occur on sites of inflamed skin (e.g.…”

Section: Introductionmentioning

confidence: 99%

The role of aldo‐keto reductase 1C3 (AKR1C3)‐mediated prostaglandin D2 (PGD2) metabolism in keloids

Mantel

Newsome

Thekkudan

et al. 2015

Experimental Dermatology

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Keloids are progressively expanding scars, mostly prevalent in individuals of African descent. Previous data identified increased mast cell number and activation state in keloids suggesting a role in disease progression. The major eicosanoid secreted by mast cells is prostaglandin D2 (PGD2), a relatively unstable pro-inflammatory mediator which can be spontaneously converted to 15-deoxy-(Delta12,14)-prostaglandin J2(15d-PGJ2) or enzymatically metabolized to 9α,11β-PGF2 by aldo-keto reductase 1C3 (AKR1C3). In this work, we investigated the possible role of PGD2 and its metabolites in keloids using CRL1762 keloid fibroblasts (KF) and immunohistochemical staining. Our data suggested approximately 3-fold increase of tryptase-positive mast cell count in keloids compared with normal skin. Furthermore, AKR1C3 was overexpressed in the fibrotic area of keloids while relatively weak staining detected in normal skin. Metabolism of PGD2 to 9α,11β-PGF2 by both, KF and normal fibroblasts, was dependent on AKR1C3 as this reaction was attenuated in the presence of the AKR1C3 inhibitor, 2'-hydroxyflavanone, or in cells with decreased AKR1C3 expression. 15d-PGJ2, but not the other tested PGs, inhibited KF proliferation, attenuated KF-mediated collagen gel contraction and increased caspase-3 activation. In addition, treatment with 15d-PGJ2 activated P38-MAPK, induced reactive oxygen species and upregulated superoxide dismutase-1 (SOD-1). Finally, inhibition of P38-MAPK further augmented 15d-PGJ2-induced caspase-3 cleavage and attenuated its effect on SOD-1 transcription. This work suggests that localized dual inhibition of AKR1C3 and P38-MAPK may inhibit keloid progression. Inhibiting AKR1C3 activity may generate oxidative environment due to redirection of PGD2 metabolism towards 15d-PGJ2 while inhibition of P38-MAPK will sensitize keloid cells to ROS-induced apoptosis.

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Section: Introductionmentioning

confidence: 99%

The role of aldo‐keto reductase 1C3 (AKR1C3)‐mediated prostaglandin D2 (PGD2) metabolism in keloids

Mantel

Newsome

Thekkudan

et al. 2015

Experimental Dermatology

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“…What we need to do now is to pay attention to the expression level of TGF‐β1 in scar‐free repair wounds, and to the temporal and spatial dynamics of TGF‐β1 to control the homeostasis of reepithelialisation, vascularization, and inflammation . In fact, there are various means of regulating the TGF‐β1 signalling pathway, including antibodies, antagonists, and even miRNA means . However, using antagonists of TGF‐β1 receptors or TGF‐β1 specific antibodies could merely reach clinical request due to the safety accidents .…”

Section: Biotherapy Aimed At Main Cytokines and Protein Involved In Hssmentioning

confidence: 99%

Biological approaches for hypertrophic scars

Zhong

2019

International Wound Journal

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Scar formation is usually the pathological consequence of skin trauma. And hypertrophic scars (HSs) frequently occur in people after being injured deeply. HSs are unusually considered as the result of tissue contraction and excessive extracellular matrix component deposition. Myofibroblasts, as the effector cells, mainly differentiated from fibroblasts, play the crucial role in the pathophysiology of HSs. A number of growth factors, inflammatory cytokines involved in the process of HS occurrence. Currently, with in‐depth exploration and clinical research of HSs, various creative and effective treatments budded. In here, we summarize the progress in the molecular mechanism of HSs, and review the available biotherapeutic methods for their pathophysiological characteristics. Additionally, we further prospected that the comprehensive therapy may be more suitable for HS treatment.

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“…La fisiopatología del proceso de cicatrización queloide es complejo, ya que involucra factores genéticos y ambientales 50 . Los fibroblastos atípicos han demostrado un papel clave durante la primera etapa.…”

Section: Participación De Las Mmps En La Generación De Cicatrices Hipunclassified

Metaloproteinasas de la matriz extracelular y su participación en el proceso de cicatrización

Ferranti-Ramos

Garza-Garza

Bátiz-Armenta

et al. 2017

revmed

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RESUMENIntroducción: las metaloproteinasas son enzimas fundamentales para el mantenimiento estructural de la matriz extracelular, así como para su degradación en situaciones donde se requiere un proceso de reparación tisular. Objetivo: realizar una revisión de los aspectos más actuales de las metaloproteinasas y su papel en la cicatrización. Metodología de búsqueda: se realizó una revisión de 95 artículos, durante el período comprendido entre el 18 de julio de 2015 y 20 de septiembre de 2016 se utilizó las bases de datos Medline, Scopus, Scielo y Science Direct. Resultados: existen seis subfamilias de metaloproteinasas: colagenasas, estromalisinas, elastasas, gelatinasas, matrilisinas y las metaloproteinasas asociadas a la membrana plasmática. Las células endoteliales vasculares las secretan en donde hay daño epitelial y se requiere de un proceso de cicatrización. Conclusiones: las metaloproteinasas son endopeptidasas dependientes de zinc fundamentales para el mantenimiento y degradación de la matriz extracelular. Cuando el mecanismo de regulación falla y las metaloproteinasas tienen una sobreexpresión, ocurren procesos de cicatrización deficientes, condicionando la aparición de heridas crónicas, cicatrices hipertróficas o queloides, pterigión, fibrosis pulmonar y hepática, entre otras condiciones. Revisión de Tema DermatologíaArtículo recibido el 29 de diciembre de 2016 y aceptado para publicación el 22 de marzo de 2017Metaloproteinasas de la matriz extracelular y su participación en el proceso de cicatrización

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Update on Keloid Management: Clinical and Basic Science Advances

Abstract: Latest discoveries in the use of novel agents suggest therapeutic alternatives for the prevention of recurrences of hypertrophic scars and postexcision keloid lesions.

Cited by 35 publications

References 29 publications

The role of aldo‐keto reductase 1C3 (AKR1C3)‐mediated prostaglandin D2 (PGD2) metabolism in keloids

The role of aldo‐keto reductase 1C3 (AKR1C3)‐mediated prostaglandin D2 (PGD2) metabolism in keloids

Biological approaches for hypertrophic scars

Metaloproteinasas de la matriz extracelular y su participación en el proceso de cicatrización

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