Transcriptomic meta-analysis characterizes molecular commonalities between psoriasis and obesity.

Genes Immun

Laboratory of Genetics, Section of Genetics, Cell Biology and Development, Department of Biology, University of Patras, 26504, Patras, Greece.

Published: June 2024

Despite the abundance of epidemiological evidence for the high comorbid rate between psoriasis and obesity, systematic approaches to common inflammatory mechanisms have not been adequately explored. We performed a meta-analysis of publicly available RNA-sequencing datasets to unveil putative mechanisms that are postulated to exacerbate both diseases, utilizing both late-stage, disease-specific meta-analyses and consensus gene co-expression network (cWGCNA). Single-gene meta-analyses reported several common inflammatory mechanisms fostered by the perturbed expression profile of inflammatory cells. Assessment of gene overlaps between both diseases revealed significant overlaps between up- (n = 170, P value = 6.07 × 10) and down-regulated (n = 49, P value = 7.1 × 10) genes, associated with increased T cell response and activated transcription factors. Our cWGCNA approach disentangled 48 consensus modules, associated with either the differentiation of leukocytes or metabolic pathways with similar correlation signals in both diseases. Notably, all our analyses confirmed the association of the perturbed T helper (Th)17 differentiation pathway in both diseases. Our novel findings through whole transcriptomic analyses characterize the inflammatory commonalities between psoriasis and obesity implying the assessment of several expression profiles that could serve as putative comorbid disease progression biomarkers and therapeutic interventions.

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http://dx.doi.org/10.1038/s41435-024-00271-wDOI Listing

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