Regulatory role of transcription factor c-Myc in the pathogenesis of psoriasis

TL;DR

This review explores how the c-Myc transcription factor contributes to psoriasis by driving skin cell overgrowth and metabolic changes.

Contribution

The paper reviews novel insights into c-Myc's regulatory role in psoriasis pathogenesis and its clinical relevance.

Findings

c-Myc is highly expressed in psoriatic lesions and linked to keratinocyte hyperproliferation.

c-Myc contributes to metabolic reprogramming in psoriasis, worsening epidermal overgrowth.

The review highlights c-Myc's role in maintaining abnormal epidermal dynamics in psoriasis.

Abstract

Psoriasis is a chronic relapsing dermatosis characterized by hyperproliferation and poor differentiation of keratinocytes (KCs). The c-Myc gene is one of the main members of the Myc family and exerts multiple biological functions. C-Myc is highly expressed in psoriatic lesions. The co-expressed genes and coexisting factors of c-Myc determine the final survival of cells. The high expression levels of c-Myc in the skin lesions of psoriatic patients are associated with the continuous proliferation of KCs, and form an abnormal state of epidermal dynamics. C-Myc is also involved in the induction of metabolic reprogramming of cells in the development of psoriasis, thus exacerbating the excessive proliferation of psoriatic epidermis. In this review, we focus on the mechanisms of the transcription factor c-Myc in the pathogenesis of psoriasis and its clinical implications.

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