Analysis of communal Pathogenesis and Immune Infiltration Characteristics Between Psoriasis and Pulmonary Arterial Hypertension

Abstract

Abstract Background Increasingly evidence has shown pulmonary arterial hypertension (PAH) was predisposed to occur in psoriasis, however, the common mechanism of this phenomenon is still not fully clarified. This study aims to further explore the molecular mechanisms of this complication. Methods Four datasets were downloaded from the Gene Expression Omnibus (GEO) database based on the study inclusion/exclusion criteria. After screening the communal DEGs, modules, and hub genes of psoriasis and PAH, subsequent bioinformatic analyses, consisting of function annotation analysis, co-expression analysis, drug-gene interaction prediction, and mRNA–miRNA regulation network construction were conducted. Moreover, Immune cell infiltration analysis and correlation analysis were performed to further uncover the related immune pathogenesis in psoriasis and PAH. Results 170 communal DEGs, 4 modules, and 6 hub genes were identified between GSE15197 and GSE30999, and the expression of hub genes was verified in the GSE41662 and GSE113439 respectively. The function annotation analysis of these genes mainly enriched in the Immune System and associated signal transduction, and the immune cell infiltration analysis highlighted the existence of the overlap in terms of mast cells between PAH and psoriasis. Conclusions The analysis of communal DEGs, modules, and hub genes underlined the potential role of the immune system and associated signal transduction in the common pathogenesis of psoriasis and PAH, and immune Infiltration analysis of two diseases provide us with new perspectives and exploring direction. Moreover, six hub genes (MYO5A, CDT1, ASPM, ACTR2, PTPN11, and SOST) may be used as biomarkers or therapeutic targets in psoriasis and PAH.