Abstract
Abstract Psoriasis is a chronic immune-mediated inflammatory disease and is associated with numerous comorbidities such as psoriatic arthritis, cardiovascular disease, metabolic syndrome, and depression. Psoriasis causes a huge burden for both individuals and society worldwide. Although significant progress has been made in psoriasis research and treatment modalities over the last decades, there is currently no cure for psoriasis. The current psoriasis treatment options are intended to control symptoms and facilitate disease going into remission. Thus, a deep understanding of the complex molecular mechanism of psoriasis is required to develop novel molecular therapies that can prevent comorbidities. In this study, we investigated the proteomic profile of high-abundance protein-depleted plasma from 30 individuals to identify molecular signatures and pathways involved in psoriasis depending on the severity of the disease. Our initial findings show that 160 proteins are significantly upregulated in active disease compared with healthy individuals. These proteins are majorly involved in platelet aggregation, platelet activation, coagulation and cell adhesion. Interestingly, proteins involved in oxidative stress, cell adhesion and metabolic processes are downregulated in inactive disease compared with healthy volunteers. Overall, this study may provide insights into systemic proteomic response to inflammation in psoriasis.
Published Version
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