treatyourscars Keloid scar is defined as a skin lesion that spreads along the edge of the original wound and continues to grow over time does not regress after the excision and is present for at least one year. Keloid scars are a familial disease and occur in all ethnic groups with dark skin. A higher incidence of keloids is found in black populations, whereas the incidence in samples of black Africans is estimated at 4-6% to 16%.
Due to the increased family aggregation and high prevalence of certain racial parallelisms (identical twins), changes in gene expression may promote the contribution of genetic risk factors to the development of keloid scars, and some researchers have suggested that the heredity of keloid scars may be autosomal recessive, although not a single gene has been identified.
As a growing familial aggregate, higher prevalence in certain breeds, parallelism in identical twins and changes in gene expression favor the remarkable genetic contribution to keloid pathology. Several genes were involved in the etiology of keloids, but not a single gene mutation was found to be responsible. It seems that the environment triggers abstract keloid diseases in susceptible individuals.
Further studies are needed to investigate the role of epigenetics in keloid etiology. The aim of this study is to identify the genes and find out how they are responsible for keloid formation. A combination of methods such as gene association, gene interactions, epigenetic links, gene expression and protein analysis can be used to determine the etiology of keloid disease.
Keloid formation and progression are associated with a variety of genetic and epigenetic factors. A genetic predisposition is suggested by the fact that keloids are more common in dark-tailed individuals, particularly Asians. The tendency to develop keloids runs in families, suggesting a possible genetic basis.
Recent studies suggest that a variety of epigenetic mechanisms promote keloid formation. The formation of keloids may be due to a failure of base switching normalization during the reconstruction phase of wound healing, said Greg Goodman, M.D., associate professor of dermatology at Monash University in Clayton, Victoria, Australia. He spoke about the subject at the World Congress of Dermatology in Milan.
According to Dr. Goodman, the wound healing process is on a continuum that passes from scar-less fetal wound healing to adult wound healing and finally to keloidal wound healing. Wound healing in adults without scars is considered normal, while keloid wound healing is characterized by uncontrolled and persistent proliferation of scar tissue.
Hypertrophic scars can occur in both sexes and ethnicities and can be caused by various forms of physical and chemical injuries such as piercings and harsh smells. Unlike keloids, hypertrophic scars are usually small, so they can disappear by themselves over time.
The benefits of removing large keloids outweigh the risks of post-operative scars. Keloids are a form of skin damage such as surgery, incisions, piercings, burns, chickenpox and acne. It is possible to prevent keloid forms by taking measures to protect the skin from skin damage.
According to the US National Center for Biotechnology Information, keloid scars are most prevalent among young people between the ages of 10 and 20. In the United States, in 15% of cases, keloid scars occur in people of sub-Saharan African descent and people of European descent. Studies have also shown that people with darker skin tones have a higher risk of keloid scars as a result of skin trauma.
Keloid scars occur in 15-20% of people with sub-Saharan African, Asian, and Latin American ancestry, as well as in people of Caucasian origin. Previously it was believed that people with albinism did not have keloids [5], but recent reports have described the frequency of keloids in Africans with albinism.
Although no single gene has been identified as the cause or factor of keloid scarring, several susceptibility sites have been discovered on chromosome 15. The study is the first to show that the altered ancestor gene plays a significant biological role in keloid development. Researchers at the Henry Ford Hospital in Detroit have identified a gene that could allow a better understanding of the development of keloid scars and open the door to improving the treatment of these diseases.
The above studies provide evidence that the regulation of DNA methylation is a stable pattern of differential gene expression during keloid formation (Table 2). As an ubiquitous alternative mechanism of gene regulation in keloid pathogenesis, DNA methylation has the ability to become a novel potential therapy for reversing destructive epigenetic modifications.
Keloid fibroblasts have been shown to overexpress collagen A (PAI-1). Short interfering RNA-targeted treatment resulted in a reduction of collagen deposition as shown in PAI-2, and targeted sIRNA interference could be a therapeutic alternative to keloid formation [99]. Short-interfering RNA inhibits the STAT3 signal converter and activator of transcription-3 expression and subsequent phosphorylation, leading to a reduction in collagen synthesis, cell proliferation and migration of keloid-derived fibroblasts, indicating a therapeutic candidate for the treatment of keloids.
Persons with III-7 hypertrophic scars carrying this haplotype are strongly separated by keloid susceptibility (Figure 2). Specific Mirna, which regulate keloids in tissues, are also involved in regulating keloid formation. Downregulation of MIR-196A is one of the mechanisms by which collagen is deposited in the keloids, and analysis by tissue reporters showed that the MIR 196A upregulation reduces the expression of collagen KFS, which binds to 3UTR in Col1a1 and Col3a1 (71).
Keloids are benign, hyperproliferative growths of dermal fibroblasts characterized by excessive deposition of extracellular matrix components (e.g. Collagen, fibronectin, elastin, proteoglycans) and growth factors such as transforming growth factors (TGF-b) (1). We think that hypertrophic scars are part of the keloid spectrum and that common pathways and genes are involved in the development of keloids and hypertrophic scars.
The scar is bumpy and raised over several months and does not grow beyond the edge of the wound. In some cases, additional scar tissue grows and forms smooth, hard growths called keloids. The distinction between small keloid and hypertrophic scars is difficult.
The development and expressivity vary due to environmental factors and genetic modifiers such as hormone status at the time of injury, inflammation and somatic variants affecting the skin and certain parts of the body when skin is exposed to UV radiation or chemical impacts. Furthermore, the degree of penetrance of certain gene variants can separate keloid families. Given the large age range at which keloids can develop in a family, genetically unaffected individuals can carry ASAH1 variants, while individuals with III-10, III-12 and III-19 can develop keloids later in life.
