TREATMENT OF PSORIASIS BY REGULATING PURINERGIC RECEPTORS

Abstract

Psoriasis is a chronic inflammatory skin disease characterized by keratinocyte hyperproliferation and immune cell infiltration. Current treatments often have limitations, including side effects and lack of long-term efficacy, highlighting the need for novel therapeutic strategies. Purinergic signaling, mediated by extracellular nucleotides and nucleosides acting on P1 (adenosine) and P2 (ATP, ADP, UTP, UDP) receptors, plays crucial roles in inflammation, immunity, and cell proliferation – processes central to psoriasis pathogenesis. This article explores the potential of targeting purinergic receptors as a therapeutic approach for psoriasis. Based on simulated in vitro and in vivo studies, our hypothetical findings suggest that modulating specific purinergic receptor subtypes (e.g., inhibiting certain P2 receptors like P2X7 or P2Y subtypes, or activating certain P1 receptors like A2A) can significantly suppress pro-inflammatory cytokine production, reduce immune cell activation, and inhibit keratinocyte hyperproliferation. Simulated data from an imiquimod-induced psoriasis-like mouse model indicate that administration of hypothetical purinergic receptor modulators reduces skin inflammation, epidermal thickness, and inflammatory infiltrate. These simulated results support the growing evidence for the involvement of the purinergic system in psoriasis and suggest that pharmacological targeting of specific purinergic receptors holds promise as a novel therapeutic avenue for this debilitating condition. Further real-world research, including preclinical validation and clinical trials, is warranted to translate these hypothetical findings into effective treatments.