Psoriasis Comorbidities and Shared Disease Mechanisms – An Investigation using Systems Biology approaches

Abstract

Comorbidity, or co-existing diseases and disorders, often contribute to the patient's overall burden. Psoriasis is a unique example of this. Investigating comorbidities in psoriasis patients is a time-consuming, laborious, and expensive process. To avoid these demerits, it is ideal to detect the possible comorbidities by exploiting the information from datasets deposited in NCBI. Once the comorbidities are identified through bio tools, they can be verified in patients with the required experimental tests. Patients with psoriasis will be able to receive better treatment because of these findings. Hence, in this study, we have utilized the Network Analyst tool to identify the comorbidities associated with psoriasis. We are reporting the protein interaction of fifteen subnetworks, whose GO CC and Reactome pathways were investigated. Notably, subnetwork 2 was involved in xenobiotic metabolism and GABA synthesis. Subnetworks 3, 9, 10, and 13 were associated with the synthesis of sphinganine, galanin, circadian proteins, and urea, respectively. Subnetwork 4 proteins synthesized bile acids and 25-hydroxy cholesterol, whereas subnetworks 7 and 16 produced chemokines, CXCL10 and CXCL1 respectively. The later subnetworks along with subnetwork 9 were involved in G alpha (i) signaling events. Due to the up-regulation of certain proteins in these subnetworks, they cause various types of diseases. The development of comorbidities from these subnetworks is lime lighted.