Abstract
BackgroundComplex chronic diseases are usually not caused by changes in a single causal gene but by an unbalanced regulating network resulting from the dysfunctions of multiple genes or their products. Therefore, network based systems approach can be helpful for the identification of candidate genes related to complex diseases and their relationships. Axial spondyloarthropathy (SpA) is a group of chronic inflammatory joint diseases that mainly affect the spine and the sacroiliac joints. The pathogenesis of SpA remains largely unknown.ResultsIn this paper, we conducted a network study of the pathogenesis of SpA. We integrated data related to SpA, from the OMIM database, proteomics and microarray experiments of SpA, to prioritize SpA candidate disease genes in the context of human protein interactome. Based on the top ranked SpA related genes, we constructed a SpA specific PPI network, identified potential pathways associated with SpA, and finally sketched an overview of biological processes involved in the development of SpA.ConclusionsThe protein-protein interaction (PPI) network and pathways reflect the link between the two pathological processes of SpA, i.e., immune mediated inflammation, as well as imbalanced bone modelling caused new boneformation and bone loss. We found that some known disease causative genes, such as TNFand ILs, play pivotal roles in this interaction.
Highlights
Complex chronic diseases are usually not caused by changes in a single causal gene but by an unbalanced regulating network resulting from the dysfunctions of multiple genes or their products
It was noticed that three major signaling pathways were responsible for mediating Tolllike receptor (TLR)-induced responses including NF-kB, mitogen-activated protein kinases (MAPKs), and IFN regulatory factors (IRFs) [46], while we found that the two pathways, MAPKs and NF-kB, which play central roles in induction of a proinflammatory response, are involved in SpA
We have extracted data related to SpA - known SpA causative genes from the Online Mendelian Inheritance in Man (OMIM) database, proteomic experiments from literature, and microarray experiments from the Gene Expression Omnibus (GEO) database
Summary
Complex chronic diseases are usually not caused by changes in a single causal gene but by an unbalanced regulating network resulting from the dysfunctions of multiple genes or their products. Axial spondyloarthropathy (SpA) is a group of chronic inflammatory joint diseases that mainly affect the spine and the sacroiliac joints. Axial spondyloarthropathy (SpA) is a family of chronic inflammatory joint diseases of the spine and the sacroiliac joints. The two central features of SpA are inflammation and new bone formation, especially in the spine [1]. There is new bone formation in the ligament, causing the thickening or hardening of the underlying bone, and eventually the fusion of the vertebral bodies and even the spinal stiffness. It is known that SpA is associated with multiple genes, such as HLA-
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