Researchers from the University of Cincinnati have published findings that may signal a potential new approach for the treatment of keloids. Focusing on the enzyme CYP24A1 involved in vitamin D metabolism, the research may help clinicians manage these disfiguring scars that extend beyond the original wound boundaries.
Published in Burns & Trauma, the study findings show a significant overexpression of CYP24A1 in keloid keratinocytes at both mRNA and protein levels. The researchers think this discovery opens up new possibilities for targeted therapies, since inhibiting the CYP24A1 enzyme could potentially mitigate the formation and progression of keloids.
In the study, primary keratinocytes were isolated from both normal and keloid skin samples. These cells were then cultured with and without vitamin D, and in the presence of CYP24A1 inhibitors (ketoconazole and VID400), permitting comprehensive assessment of gene expression and cell behaviour under different treatment scenarios.
Results showed that:
Ketoconazole produced a broad reduction in cell proliferation;
VID400 specifically targeted keloid keratinocyte growth without affecting migration;
Both inhibitors effectively suppressed the expression of profibrotic genes, including periostin and hyaluronan synthase 2; and
The combination of these inhibitors with vitamin D amplified gene-specific effects.
According to a press release, the implications of these findings extend beyond immediate clinical applications. By spotlighting CYP24A1 as a critical player in keloid pathology, the research adds to a growing body of evidence implicating vitamin D signalling pathways in the regulation of wound healing and scarring, and suggest that CYP24A1 inhibition may serve as potential adjunct therapy for keloids.
The research also contributes to the broader understanding of vitamin D's role in wound healing and scar formation. The authors believe this could lead to more tailored and effective therapies, potentially improving the quality of life for individuals affected by keloids.
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