Genetics of keloid scarring

Shih, Barbara; Bayat, Ardeshir

doi:10.1007/s00403-009-1014-y

Cited by 238Dermatologic Treatments and ResearchGenetic and rare skin diseases.Dupuytren's Contracture and Treatments

Genetics of keloid scarring

Shih, Barbara, Bayat, Ardeshir·2010·Archives of Dermatological Research

DOI 10.1007/s00403-009-1014-y

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Abstract

Keloid scarring, also known as keloid disease (KD), is a common, abnormally raised fibroproliferative cutaneous lesion that can occur following even minor skin trauma. The aetiopathogenesis of KD has remained an enigma todate compounded by an ill-defined clinical management. There is strong evidence suggesting a genetic susceptibility in individuals affected by KD, including familial heritability, common occurrence in twins and high prevalence in certain ethnic populations. This review aims to address the genetic aspects of KD that have been described in present literature that include inheritance patterns, linkage studies, case-control association studies, whole genome gene expression microarray studies and gene pathways that were significant in KD. In addition to our clinical and scientific background in KD, we used search engines, Scopus, Scirus and PubMed, which searched for key terms covering various genetic aspects of KD. Additionally, genes reported in seven whole genome gene expression microarray studies were separately compared in detail. Our findings indicate a varied inheritance pattern in KD (predominantly autosomal dominant), linkage loci (chromosomes 2q23 and 7p11), several human leukocyte antigen (HLA) alleles (HLA-DRB1*15, HLA-DQA1*0104, DQ-B1*0501 and DQB1*0503), negative candidate gene case-control association studies and at least 25 dysregulated genes reported in multiple microarray studies. The major pathways reportedly proposed to be involved in KD include apoptosis, mitogen-activated protein kinase, transforming growth factor-beta, interleukin-6 and plasminogen activator inhibitor-1. In summary, involvement of more than one gene is likely to be responsible for susceptibility to KD. A better understanding of the genes involved in KD may potentially lead to the development of more effective diagnostic, therapeutic and prognostic measures.

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Genetic susceptibility to keloid disease: Transforming growth factor β receptor gene polymorphisms are not associated with keloid disease
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Wound repair and regeneration: Mechanisms, signaling, and translation
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Cellular and molecular mechanisms of repair in acute and chronic wound healing
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The Keloid Disorder: Heterogeneity, Histopathology, Mechanisms and Models
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Extracellular matrix molecules implicated in hypertrophic and keloid scarring
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The Role of Extracellular Matrix in Skin Wound Healing
Potekaev, N., Borzykh, O., Medvedev, G. V., Pushkin, D., Petrova, M., Petrov, A. V., Dmitrenko, D., Karpova, E. I., Demina, O., & Shnayder, N. (2021) · Journal of Clinical Medicine · doi:10.3390/jcm10245947 · Cited by 189 · see citing works
Keloids and Hypertrophic Scars: A Spectrum of Clinical Challenges
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Fibroblasts from the growing margin of keloid scars produce higher levels of collagen I and III compared with intralesional and extralesional sites: clinical implications for lesional site-directed therapy
Syed, F., Ahmadi, E., Iqbal, S. A., Singh, S., McGrouther, D. A., & Bayat, A. (2010) · British Journal of Dermatology · doi:10.1111/j.1365-2133.2010.10048.x · Cited by 174 · see citing works
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Understanding Keloid Pathobiology From a Quasi-Neoplastic Perspective: Less of a Scar and More of a Chronic Inflammatory Disease With Cancer-Like Tendencies
Tan, S., Khumalo, N. P., & Bayat, A. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.01810 · Cited by 173 · see citing works
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Asiaticoside suppresses collagen expression and TGF-β/Smad signaling through inducing Smad7 and inhibiting TGF-βRI and TGF-βRII in keloid fibroblasts
Tang, B., Zhu, B., Liang, Y., Bi, L., Hu, Z., Chen, B., Zhang, K., & Zhu, J. (2011) · Archives of Dermatological Research · doi:10.1007/s00403-010-1114-8 · Cited by 151 · see citing works
Current Understanding of the Genetic Causes of Keloid Formation
Glass, D. A. (2017) · Journal of Investigative Dermatology Symposium Proceedings · doi:10.1016/j.jisp.2016.10.024 · Cited by 140 · see citing works
miR-196a Downregulation Increases the Expression of Type I and III Collagens in Keloid Fibroblasts
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Keloid Scarring: Understanding the Genetic Basis, Advances, and Prospects
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A comprehensive evidence-based review on the role of topicals and dressings in the management of skin scarring
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Keloids: Current and emerging therapies
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The role of macrophages in the formation of hypertrophic scars and keloids
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Insights into the Pathophysiology of Hypertrophic Scars and Keloids: How Do They Differ?
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Current Advances in Hypertrophic Scar and Keloid Management
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Keloid‐derived keratinocytes exhibit an abnormal gene expression profile consistent with a distinct causal role in keloid pathology
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Cellular and Molecular Characteristics of Scarless versus Fibrotic Wound Healing
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Mechanosignaling pathways in cutaneous scarring
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Comparative wound healing—Are the small animal veterinarian's clinical patients an improved translational model for human wound healing research?
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Therapeutic potential of fibroblast growth factor-2 for hypertrophic scars: upregulation of MMP-1 and HGF expression
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German S2k guidelines for the therapy of pathological scars (hypertrophic scars and keloids)
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Epidermal Notch1 recruits RORγ+ group 3 innate lymphoid cells to orchestrate normal skin repair
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Authors: Shih, B., & Bayat, A.
Affiliations: University of Manchester (GB)
Corresponding author: Bayat, Ardeshir
ORCID: Shih, Barbara
Bayat, Ardeshir
Venue: Archives of Dermatological Research
Publisher: Springer Science and Business Media LLC
Published: 2010-02-04
Volume: 302
Issue: 5
Pages: 319-339
ISSN: 0003-9187 (ISSN-L)
0340-3696
1432-069X
DOI: 10.1007/s00403-009-1014-y
OpenAlex: W2025153976
Cited by: 238
References: 153
Citations by year: 2026: 7 · 2025: 7 · 2024: 6 · 2023: 11 · 2022: 19 · 2021: 21 · 2020: 19 · 2019: 13 · 2018: 8 · 2017: 22 · 2016: 16 · 2015: 11 · 2014: 21 · 2013: 16 · 2012: 15
FWCI: 3.14
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Archives of Dermatological Research (publishedVersion)
PubMed (publishedVersion)
Lancaster EPrints (Lancaster University) (submittedVersion)
UCL Discovery (University College London) (submittedVersion)
Research Explorer (The University of Manchester) (submittedVersion)
Topics: Health Sciences › Medicine › Dermatology › Dermatologic Treatments and Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic and rare skin diseases.
Health Sciences › Medicine › Rheumatology › Dupuytren's Contracture and Treatments
Keywords: keloids, genetic susceptibility, mode of inheritance, autosomal dominant inheritance, genetic linkage, HLA alleles, HLA-DRB1*15, gene expression microarrays, dysregulated genes, apoptosis, mitogen-activated protein kinase, TGF-beta, interleukin-6, plasminogen activator inhibitor-1, ethnic predisposition
MeSH terms: Cicatrix, Clinical Trials as Topic, HLA Antigens, Humans, Keloid, Polymorphism, Genetic, Transforming Growth Factor beta, Apoptosis, Plasminogen Activator Inhibitor 1, Genetic Predisposition to Disease, Oligonucleotide Array Sequence Analysis, Mitogen-Activated Protein Kinases, Inheritance Patterns, Genome-Wide Association Study

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Genetics of keloid scarring

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