Cardiovascular complications combined with COVID-19 (SARS-CoV-2) lead to a poor prognosis in patients. The common pathogenesis of ischemic cardiomyopathy (ICM) and COVID-19 is still unclear. Here, we explored potential molecular mechanisms and biomarkers for ICM and COVID-19. Common differentially expressed genes (DEGs) of ICM (GSE5406) and COVID-19 (GSE164805) were identified using GEO2R. We performed enrichment and protein–protein interaction analyses and screened key genes. To confirm the diagnostic performance for these hub genes, we used external datasets (GSE116250 and GSE211979) and plotted ROC curves. Transcription factor and microRNA regulatory networks were constructed for the validated hub genes. Finally, drug prediction and molecular docking validation were performed using cMAP. We identified 81 common DEGs, many of which were enriched in terms of their relation to angiogenesis. Three DEGs were identified as key hub genes (HSP90AA1, HSPA9, and SRSF1) in the protein–protein interaction analysis. These hub genes had high diagnostic performance in the four datasets (AUC > 0.7). Mir-16-5p and KLF9 transcription factor co-regulated these hub genes. The drugs vindesine and ON-01910 showed good binding performance to the hub genes. We identified HSP90AA1, HSPA9, and SRSF1 as markers for the co-pathogenesis of ICM and COVID-19, and showed that co-pathogenesis of ICM and COVID-19 may be related to angiogenesis. Vindesine and ON-01910 were predicted as potential therapeutic agents. Our findings will contribute to a deeper understanding of the comorbidity of ICM with COVID-19.

Objective: To investigate the molecular mechanism and simulated validation of Zhi Bai Di Huang Pill (ZBDHP) for the treatment of systemic lupus erythematosus (SLE) using network pharmacology and molecular docking techniques. Methods: The active ingredients of ZBDHP were obtained through the TCMSP database and the Canonical SMILES of the active ingredients were queried through Pubchem. The targets of the active ingredients were predicted in the SwissTarget database based on the SMILES. The SLE-related disease targets were obtained through the GeneCards, OMIM and DisGenets databases, and the intersection targets of ZBDHP and SLE were obtained using the Venny 2.1.0 online platform. Intersection targets build a visual protein interaction network (PPI) through the STRING database, and the core targets were identified by network topology analysis. GO analysis and KEGG pathway enrichment analysis of the intersecting targets were performed using the DAVID database. Finally, the molecular docking of the first four active ingredients and the first four core target genes were verified by Pubchem, the PDB database and CB-Dock online molecular docking technology. Results: ZBDHP screened 91 potential active ingredients and 816 potential targets. Among them, 141 genes were intersected by ZBDHP and SLE. The network topology analysis showed that the main active ingredients were Hydroxygenkwanin, Alisol B, asperglaucide, Cerevisterol, etc., and the key target genes were TNF, AKT1, EGFR, STAT3, etc. GO and KEGG enrichment analysis showed that common targets interfere with biological processes or molecular functions such as signal transduction protein phosphorylation, inflammatory response, transmembrane receptor protein tyrosine kinase activity, etc., through multiple signaling pathways, such as pathways in cancer, Kaposi sarcoma-associated herpesvirus infection, the PI3K-Akt signaling pathway, lipid and atherosclerosis, hepatitis B, etc. Molecular docking results showed that the active components of ZBDHP have good binding activity to the core targets of SLE. Conclusions: This study reveals that the ZBDHP treatment of SLE is a complex mechanistic process with multi-components, multi-targets and multi-pathways, and it may play a therapeutic role in SLE by inhibiting the production, proliferation and apoptosis of inflammatory factors. In conclusion, the present study provides a theoretical basis for further research on ZBDHP.

Background: Qianghuo Shengshi decoction (QHSSD), a traditional Chinese medicine formula, is used to treat ankylosing spondylitis (AS) in China. The pharmacological mechanism of QHSSD for AS remains to be clarified. In this study, we investigated the molecular mechanisms of QHSSD in the treatment of AS using network pharmacology and molecular docking. Methods: To obtain the chemical components and potential targets of QHSSD, we used the Traditional Chinese Medicine Systematic Pharmacology Database and Analysis Platform (TCMSP) and SwissTargetPrediction. AS potential targets were found in the GeneCards, OMIM, and DisGenets databases. A Venn diagram was used to screen QHSSD and AS common potential targets. The STRING website and Cytoscape software were used to create and analyze protein–protein interactions and component–target networks. The DAVID database was used for the gene ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Molecular docking was used to visualize drug–target interactions. Results: The component–target network consisted of 119 chemical components and 193 potential targets. QHSSD was implicated in various biological processes, such as inflammation and angiogenesis, and mediated multiple signaling pathways, such as the MAPK signaling pathway. Molecular docking revealed good binding ability between medicarpin, notoptol, vitetrifolin E, and cnidilin and EGFR, TNF-α, ALB, and VEGFA. Conclusions: The chemical compositions, potential targets, and pathways involved in the QHSSD treatment of AS were successfully predicted in this study. This study provides a solid foundation for the selection of drugs to treat AS.