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Objective To screen the differentially expressed genes (DEGs) of ankylosing spondylitis (AS) by bioinformatic analysis and make literature review for their functions. Methods The data about genome microarray of AS were retrieved from the Gene Expression Omnibus (GEO) database, and then employed to screen out DEGs between synovial biopsies from AS and undifferentiated spondylitis patients and the samples from healthy individuals and osteoarthritis patients by GEO2R. The DEGs were then subjected to Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis in DAVID 6.8 database. Finally, protein-protein interaction (PPI) network was constructed by STRING10.5 and then further analyzed by the Cytoscape software. Results A total of 190 differential genes were screened out, of which 75 were up-regulated and 115 were down-regulated. GO analysis showed that the obtained DGEs were mainly involved in inflammatory response, leukocyte migration, extracellular domain, extracellular region, extracellular matrix, lipoprotein particle binding and carbohydrate binding. KEGG analysis suggested that these DGEs were enriched in rheumatoid arthritis and cytokine-cytokine receptor interaction, and others. The PPI network was constructed by STRING database. And then, with the aid of Cytoscape, 12 Hub genes with highest degree of ankylosing spondylitis (including CXCR4, SELL, CD79A, MMP3, CD68, ADIPOQ, CCL19, IL-7R, IL-1β, MYH14, APOE and FCGR3A) were screened out. What's more, 41 transcription factors (TFs) interacting with the above 12 Hub genes, including ETS1, GATA3, IRF8 and so on were screened out with the iRegulon, a plugin in Cytoscape. Conclusion The firstly selected 12 Hub genes and 41 TFs may play important roles in pathogenesis of AS, and are regarded as new biomarkers for the diagnosis and treatment for AS.

Coronavirus disease‐19 (COVID‐19) is caused by severe acute respiratory syndrome‐coronavirus‐2 (SARS‐CoV‐2) infection. The COVID‐19 pandemic began in March 2020 and has wrought havoc on health and economic systems worldwide. Efficacious treatment for COVID‐19 is lacking: Only preventive measures as well as symptomatic and supportive care are available. Preclinical and clinical studies have indicated that lysosomal cathepsins might contribute to the pathogenesis and disease outcome of COVID‐19. Here, we discuss cutting‐edge evidence on the pathological roles of cathepsins in SARS‐CoV‐2 infection, host immune dysregulations, and the possible underlying mechanisms. Cathepsins are attractive drug targets because of their defined substrate‐binding pockets, which can be exploited as binding sites for pharmaceutical enzyme inhibitors. Accordingly, the potential modulatory strategies of cathepsin activity are discussed. These insights could shed light on the development of cathepsin‐based interventions for COVID‐19. [ABSTRACT FROM AUTHOR]