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

The DOI matches its Crossref record; 153 of the 153 references it cites were found in a registry or an index.

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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Crossref · 10.1007/s00403-009-1014-y

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  1. Zhuo Y, Gao JH, Luo SQ, Zeng WS, Hu ZQ, Lu F, Zhao YZ (2005) p53 gene codon 72 polymorphism and susceptibility to keloid. Zhonghua Zheng Xing Wai Ke Za Zhi 21(3):201–203

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Metadata

Authors
Shih, B., & Bayat, A.
Affiliations
University of Manchester (GB)
Corresponding author
Bayat, Ardeshir
ORCID
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
  • Health Sciences › Medicine › Dermatology › 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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