Abstract
Interactions of genes in intersecting signaling pathways, as well as environmental influences, are required for the development of psoriasis. Peroxisome proliferator-activated receptor gamma (PPARγ) is a nuclear receptor and transcription factor which inhibits the expression of many proinflammatory genes. We tested the hypothesis that low levels of PPARγ expression promote the development of psoriatic lesions. We combined experimental results and network functional analysis to reconstruct the model of PPARγ-downregulated signaling in psoriasis. We hypothesize that the expression of IL17, STAT3, FOXP3, and RORC and FOSL1 genes in psoriatic skin is correlated with the level of PPARγ expression, and they belong to the same signaling pathway that regulates the development of psoriasis lesion.
Highlights
Psoriasis is an example of chronic inflammatory skin disorder with a complex multifactorial origin
Based on the literature-based protein-protein interactome (PPI) and pathway analysis, we proposed that low PPARγ activity promotes the development of psoriatic lesions due to changes in the inflammatory signaling pathways regulated by STAT3, RORC, FOXP3, FOSL1, and IL17A
For researching the downstream targets, we looked for the genes and proteins which were reported to be inhibited by PPARγ and simultaneously were positive biomarkers for psoriasis. 146 associated with psoriasis genes and gene families whose expressions are repressed by PPARγ had been found
Summary
Psoriasis is an example of chronic inflammatory skin disorder with a complex multifactorial origin. Each PSORS contains a list with several revealed genes candidates [5]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
