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This study found that sulfated CCK octapeptide reduces psoriasis-like skin inflammation in mice, suggesting a new pathophysiological role for CCK in regulating epidermal inflammation.

This study found that N,N-dimethylglycine sodium salt promoted proliferation and migration of cultured human epidermal keratinocytes and had anti-inflammatory and antioxidant effects in vitro.

This study found that deletion of c-Jun and JunB in mouse bulge hair follicle stem cells was sufficient to trigger psoriasis-like skin disease through thymic stromal lymphopoietin signaling.

In a conditional knockout mouse model, this study found that loss of the transcription elongation factor SPT6 in basal keratinocytes led to psoriasis-like skin inflammation and delayed wound healing, suggesting SPT6 plays a crucial role in maintaining epidermal immune quiescence by suppressing proinflammatory NF-κB signaling.

In this study, researchers found that the protein eIF4E is crucial for keratinocyte proliferation in psoriasis, suggesting it as a potential treatment target for the condition.