Common pathways and molecular signatures in Ankylosing Spondylitis and Psoriatic Arthritis: a perspective of systems biology.
Spondyloarthropathies; Psoriatic Arthritis; Ankylosing Spondylitis; Genes; Systems Biology
Spondyloarthropathies (SpA), also called spondyloarthritis or spondylopathies, are hereditary, inflammatory, autoimmune, chronic and rheumatic diseases with probable genetic, psychological and environmental triggers. It is a group of six rheumatic diseases with involvement of the spine and pelvis, although some forms also involve joint involvement of the arms and/or legs. The diseases classified as spondyloarthropathies are: Ankylosing spondylitis (AS); Psoriatic arthritis (PA); Reactive arthritis; Enteropathic arthritis; Undifferentiated spondyloarthropathy; Juvenile spondyloarthropathies. The two diseases investigated in this project are Psoriatic Arthritis and Ankylosing Spondylitis. They are two autoimmune diseases, with phenotypic and symptomatic overlaps, the same diagnostic method and treatments. The aim of this study is to investigate the dysregulation of molecular pathways and the regulation of differential expression of central genes for Ankylosing Spondylitis and Psoriatic Arthritis, to identify possible genetic factors and potential overlapping and specific cellular mechanisms for each syndrome. For this purpose, the gene expression profiles of AS and PsA will be analyzed to identify molecular biomarkers, genetic signatures and common pathways of both Spondyloarthritis. The gene regulatory networks with their transcription factors and target genes of each disease will also be investigated to construct the gene and protein regulatory interaction network of AS and PsA, and to identify the set of master regulators and Hubs similar to both pathologies. It is expected that the analysis with a systemic approach, starting from the overlaps in specific expression, may result in a better understanding of each syndrome, and lead to the discovery of new markers or targets for more effective treatments.