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
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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“although it is widely accepted that darker-skinned populations have a higher occurrence of keloids than lighter-skinned populations (17).”
From Wound repair and regeneration: Mechanisms, signaling, and translation (2014) · cites this paper as [17]
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Cites
Systematic and integrative analysis of large gene lists using DAVID bioinformatics resources
Huang, D. W., Sherman, B. T., & Lempicki, R. A. (2009) · Nature Protocols · doi:10.1038/nprot.2008.211 · Cited by 35,890
DAVID: Database for Annotation, Visualization, and Integrated Discovery
Dennis, G., Sherman, B. T., Hosack, D. A., Yang, J., Gao, W., Lane, H. C., & Lempicki, R. A. (2003) · Genome Biology · doi:10.1186/gb-2003-4-5-p3 · Cited by 9,327
Gurtner, G. C., Werner, S., Barrandon, Y., & Longaker, M. T. (2008) · Nature · doi:10.1038/nature07039 · Cited by 6,542
Smad-dependent and Smad-independent pathways in TGF-β family signalling
Derynck, R., & Zhang, Y. E. (2003) · Nature · doi:10.1038/nature02006 · Cited by 5,498
Thomas, A. C., & Campbell, J. H. (2000) · Cited by 2,800
Yu, Q., & Stamenkovic, I. (2000) · PubMed · Cited by 1,952
Yu, Q., & Stamenkovic, I. (2000) · Genes & Development · doi:10.1101/gad.14.2.163 · Cited by 1,754
Rubinstein-Taybi syndrome caused by mutations in the transcriptional co-activator CBP
Petrif, F., Giles, R. H., Dauwerse, H. G., Saris, J. J., Hennekam, R. C. M., Masuno, M., Tommerup, N., van Ommen, G.-J. B., Goodman, R. H., Peters, D. J. M., et al. (1995) · Nature · doi:10.1038/376348a0 · Cited by 1,217
Shah, M., Foreman, D. M., & Ferguson, M. W. J. (1995) · Journal of Cell Science · doi:10.1242/jcs.108.3.985 · Cited by 1,168
International Clinical Recommendations on Scar Management
Mustoe, T. A., Cooter, R. D., Gold, M. H., Hobbs, R. F., Ramelet, A.-A., Shakespeare, P. G., Stella, M., Téot, L., Wood, F. M., & Ziegler, U. E. (2002) · Plastic & Reconstructive Surgery · doi:10.1097/00006534-200208000-00031 · Cited by 1,081
Research works printed but not linked: 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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Wound repair and regeneration: Mechanisms, signaling, and translation
Eming, S. A., Martin, P., & Tomic-Canic, M. (2014) · Science Translational Medicine · doi:10.1126/scitranslmed.3009337 · Cited by 3,562
Cellular and molecular mechanisms of repair in acute and chronic wound healing
Martin, P. B., & Nunan, R. D. (2015) · British Journal of Dermatology · doi:10.1111/bjd.13954 · Cited by 1,183
The Keloid Disorder: Heterogeneity, Histopathology, Mechanisms and Models
Limandjaja, G. C., Niessen, F. B., Scheper, R. J., & Gibbs, S. (2020) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2020.00360 · Cited by 356
Jeschke, M. G., Wood, F. M., Middelkoop, E., Bayat, A., Téot, L., Ogawa, R., & Gauglitz, G. G. (2023) · Nature Reviews Disease Primers · doi:10.1038/s41572-023-00474-x · Cited by 229
Self-citationExtracellular matrix molecules implicated in hypertrophic and keloid scarring
Sidgwick, G. P., & Bayat, A. (2011) · Journal of the European Academy of Dermatology and Venereology · doi:10.1111/j.1468-3083.2011.04200.x · Cited by 208
Self-citation
Metadata
- Authors
- Shih, B., & Bayat, A.
- Affiliations
- University of Manchester (GB)
- Corresponding author
- Bayat, Ardeshir
- Venue
- Archives of Dermatological Research
- Published
- 2010-02-04
- Volume
- 302
- Issue
- 5
- Pages
- 319-339
- ISSN
- 0003-9187 (ISSN-L)
- 0340-3696
- 1432-069X
- 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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