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Insights into the pathogenesis of axial spondyloarthropathy from network and pathway analysis
Logistical Engineering University.
University of Missouri-Kansas City.
Logistical Engineering University.
Umeå University, Faculty of Science and Technology, Department of Physics. (IceLab)ORCID iD: 0000-0003-2156-1096
2012 (English)In: BMC Systems Biology, ISSN 1752-0509, Vol. 6, S4- p.Article in journal (Refereed) Published
Abstract [en]


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. 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.


In 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.


The 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.

Place, publisher, year, edition, pages
BioMed Central, 2012. Vol. 6, S4- p.
National Category
Microbiology in the medical area
URN: urn:nbn:se:umu:diva-57419DOI: 10.1186/1752-0509-6-S1-S4OAI: diva2:541703
Swedish Research Council, 2009-3536
Available from: 2012-08-06 Created: 2012-07-23 Last updated: 2013-09-06Bibliographically approved

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