Chronic plaque psoriasis is an inflammatory skin disease that is initiated by genetic predisposition and environmental factors. It is associated with extra-cutaneous morbidities and reduced quality of life. An unwanted transfer of signals between innate and adaptive immunity, the epithelia and the vasculature is responsible for the inflammatory setting in psoriasis. 

Even after the advancements and development of promising treatment strategies (mostly targeting the immune system), patients’ goals remain unmet. 

Vascular endothelial growth factor A (VEGF-A) mediates angiogenesis and remains upregulated in the plaques and plasma of psoriatic patients. Transgenic expression of VEGF-A in experimental models had resulted in the occurrence of psoriasis-like skin lesions. Also, in-vivo models have shown clearance of psoriasis-like inflammation on Targeting VEGF-A. 

Anti-angiogenesis treatments are commonly employed in cancer and eye disease. Clinical reports of patients treated with VEGF-A inhibitors have shown PASI improvement. Current treatments for psoriasis downregulate VEGF-A as well as angiogenesis as their therapeutic effect. 

Pharmacogenetics studies indicate the presence of various genetic signatures in psoriatic patients determines the difference in treatment responsiveness and disease severity. 

Some patients with psoriasis have an increased predisposition to produce high levels of VEGF-A. They are most likely to be benefitted from anti-VEGF-A therapy, presenting a possibility to personalize treatment in psoriasis. Anti-VEGF-A therapies are a good alternative to existing anti-cytokine strategies or can be used as an add-on to standard treatments for the management of psoriasis.

Source- Lunges-Martinez A, Paus R, Young HS. A novel personalized treatment approach for psoriasis: anti-VEGF-A therapy, BJD, 2021. https://doi.org/10.1111/bjd.20940