A new bioinformatics study offers insight into the pathogenesis of pulmonary arterial hypertension (PAH) as well as 10 newly identified hub genes that could represent potential treatment targets for the disease. The study, published in the Canadian Respiratory Journal, employed multiple microarray analyses to provide a theoretical basis for future research in PAH.

“Although basic discoveries and pivotal clinical trials have led to the development of medications in recent years, patients with PAH still have a poor prognosis,” the authors wrote. “The objective of this study was to use transcriptomic microarray data analysis to find genes associated with the onset of pulmonary hypertension, and to provide a research basis for identifying new potential therapeutic targets.”

The research team used bioinformatics analyses of 2 sets of microarray data from the National Center for Biotechnology Information (NCBI) Gene Expression Omnibus, an open-access database, to search for differentially expressed genes (DEGs) between patients with PAH and healthy controls as well as for the primary signaling pathways of those genes.

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In addition, they established a protein-protein interaction network to identify hub genes in PAH, with the aim of providing a research direction for discovering new biomarkers and therapeutic strategies.

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The results revealed 10 hub genes that could be new treatment targets: HSP90AA1, CDC5L, MDM2, LRRK2, CFTR, IQGAP1, CAND1, TOP2A, DDX21, and HIF1A. Furthermore, comparisons of the DEGs between patients and healthy individuals found that the pathways of focal adhesion, vascular smooth muscle contraction, and regulation of the actin cytoskeleton were involved in PAH.

The authors caution that these are preliminary analyses and therefore further in vitro and in vivo studies will be required to validate these findings.


Wei RQ, Zhang WM, Liang Z, Piao C, Zhu G. Identification of signal pathways and hub genes of pulmonary arterial hypertension by bioinformatic analysis. Can Respir J. 2022;2022:1394088. doi:10.1155/2022/1394088