Abstract
Keloids and non-diabetic kidney disease are both fibrotic processes that disproportionately affect persons of African descent. Despite similarities in these conditions, the authors identified no studies to date investigating a shared genetic etiology. MYH9 and APOL1 are in linkage disequilibrium and have both been associated with non-diabetic kidney disease. MYH9 codes for a non-muscle myosin that is involved in cell adhesion and locomotion and is known to be overexpressed in keloids. Variations in APOL1 confer resistance to subspecies of Trypanosoma brucei, which may explain why otherwise deleterious genetic alterations in this haplotype could have gained prominence. We feel that the pathophysiological and epidemiological overlap between keloids and non-diabetic kidney disease support a common genetic origin and further investigation into keloids and the MYH9–APOL1 haplotype and keloids is warranted. Furthermore, we feel this haplotype might offer insight into thrombosis, stroke and other conditions that disproportionately affect persons of African descent.
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