Molecular reasons for the effectiveness of Zinc in modulating Psoriasis

Psoriasis is an autoimmune skin disease characterized by excessive proliferation andabnormal differentiation of keratinocytes (۱). There is no cure for this disease. Using a study in theGEO DataSets Database that compared the expression in lesional and non-lesional skin (GSE۱۶۱۶۸۳),we separated the genes that had changed expression and filtered with logFC>۲ and Padj<۰.۰۵ andreached ۶۹ genes. Using the STRING database, we drew a network for these genes, finally we selectedone of the hub genes named Krt۱۶. Krt۱۶ is a type I keratin and plays a key role in the skin as a regulatorof innate immunity in response to skin damage (۲). In the DrugBank database, there is the drugClocortolone for this gene, and Zinc and Zinc Acetate have been introduced as targets for this protein.In a meta-analysis, it was seen that people with Psoriasis have low serum Zinc and high Copper, andthe ratio of Copper to Zinc in these people is high (۳). Overexpression of Krt۱۶ has been observed inskin diseases characterized by proliferation such as Psoriasis (۱). In addition, it has been reported thatKrt۱۶ is a marker of keratinocyte proliferation in Psoriasis in vivo and in vitro (۱). In a study, bysilencing the Krt۱۶ gene with siRNA, the ERK signaling pathway, which is responsible for cellproliferation and VEGF secretion, was turned off and the disease improved (۱). It seems that bybalancing these two elements in the patient's body, hope for recovery can be brought to these patients.

کلیدواژه ها:

Psoriasis ، Krt۱۶ ، Zinc ، Proliferation ، ERK