Recently, a study published in the journal Burns & Trauma has brought new hope for the treatment of keloid scars. The study revealed the effect of inhibiting an enzyme called CYP24A1 (which is involved in vitamin D metabolism) on keloid keratinocytes, providing new ideas and potential targets for overcoming this problem that plagues many patients.

Keloids are fibrotic scars that extend beyond the boundaries of the original wound, often causing physical disfigurement and emotional distress to patients. Their formation is closely related to the overproduction of extracellular matrix components (such as type I collagen), reflecting an imbalance in tissue repair mechanisms. However, as the molecular mechanisms behind keloid formation are not fully understood and existing treatments have limited effectiveness, patients face the dilemma of a lack of reliable treatment options.

To fill this knowledge gap, researchers at the University of Cincinnati delved deeper into the molecular drivers of keloid pathology. Using an innovative approach, they isolated primary keratinocytes from normal and keloid skin samples and cultured these cells in the presence and absence of vitamin D, while also adding the CYP24A1 inhibitors ketoconazole and VID400 to assess their effects on gene expression and cell behavior.

The results were impressive. CYP24A1 was significantly overexpressed in keloid keratinocytes at both the mRNA and protein levels. While ketoconazole broadly reduced cell proliferation, VID400 specifically targeted the growth of keloid keratinocytes without affecting their migration. In addition, both inhibitors effectively suppressed the expression of profibrotic genes such as periostin and hyaluronan synthase 2. When combined with vitamin D, the gene-specific effects of these inhibitors were further enhanced, showing potential as adjunctive treatments for keloids.

The significance of this discovery goes far beyond the clinical application itself. It further confirms the key role of CYP24A1 in the pathology of keloids and provides new and powerful evidence for the theory that the vitamin D signaling pathway is involved in the regulation of wound healing and scar formation. This new paradigm not only enriches the scientific community's understanding of keloids but may also promote the development of more precise and effective treatments, thereby significantly improving the quality of life of patients with keloids.

The results of this study mark an important step forward in the field of dermatology in the treatment of keloids. It brings new hope to patients and lays a solid foundation for the exploration of tailored and far-reaching treatment strategies in the future.