
| 10.1016/j.genrep.2022.101597
http://scihub22266oqcxt.onion/10.1016/j.genrep.2022.101597
 35317263!8931993!35317263
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Gene+Rep 2022 ; 27 (�): 101597 Nephropedia Template TP
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Using bioinformatics and systems biology to discover common pathogenetic processes between sarcoidosis and COVID-19 #MMPMID35317263Fu L; Yao M; Liu X; Zheng DGene Rep 2022[Jun]; 27 (�): 101597 PMID35317263show ga
The coronavirus disease (COVID-19) pandemic caused by SARS-CoV-2 is ongoing. Individuals with sarcoidosis tend to develop severe COVID-19; however, the underlying pathological mechanisms remain elusive. To determine common transcriptional signatures and pathways between sarcoidosis and COVID-19, we investigated the whole-genome transcriptome of peripheral blood mononuclear cells (PBMCs) from patients with COVID-19 and sarcoidosis and conducted bioinformatic analysis, including gene ontology and pathway enrichment, protein-protein interaction (PPI) network, and gene regulatory network (GRN) construction. We identified 33 abnormally expressed genes that were common between COVID-19 and sarcoidosis. Functional enrichment analysis showed that these differentially expressed genes were associated with cytokine production involved in the immune response and T cell cytokine production. We identified several hub genes from the PPI network encoded by the common genes. These hub genes have high diagnostic potential for COVID-19 and sarcoidosis and can be potential biomarkers. Moreover, GRN analysis identified important microRNAs and transcription factors that regulate the common genes. This study provides a novel characterization of the transcriptional signatures and biological processes commonly dysregulated in sarcoidosis and COVID-19 and identified several critical regulators and biomarkers. This study highlights a potential pathological association between COVID-19 and sarcoidosis, establishing a theoretical basis for future clinical trials.�
  
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