Prediction and analysis of microRNAs involved in COVID-19 inflammatory processes associated with the NF-kB and JAK/STAT signaling pathways

Abstract

COVID-19 is the cause of a pandemic associated with substantial morbidity and mortality. As yet, there is no available approved drug to eradicate the virus. In this review article, we present an alternative study area that may contribute to the development of therapeutic targets for COVID-19. Growing evidence is revealing further pathophysiological mechanisms of COVID-19 related to the disregulation of inflammation pathways that seem to play a critical role toward COVID-19 complications. The NF-kB and JAK/STAT signaling pathways are highly activated in acute inflammation, and the excessive activity of these pathways in COVID-19 patients likely exacerbates the inflammatory responses of the host. A group of non-coding RNAs (miRNAs) manage certain features of the inflammatory process. In this study, we discuss recent advances in our understanding of miRNAs and their connection to inflammatory responses. Additionally, we consider the link between perturbations in miRNA levels and the onset of COVID-19 disease. Furthermore, previous studies published in the online databases, namely web of science, MEDLINE (PubMed), and Scopus, were reviewed for the potential role of miRNAs in the inflammatory manifestations of COVID-19. Moreover, we disclosed the interactions of inflammatory genes using STRING DB and designed interactions between miRNAs and target genes using Cityscape software. Several miRNAs, particularly miR-9, miR-98, miR-223, and miR-214, play crucial roles in the regulation of NF-kB and JAK-STAT signaling pathways as inflammatory regulators. Therefore, this group of miRNAs that mitigate inflammatory pathways can be further regarded as potential targets for far-reaching-therapeutic strategies in COVID-19 diseases.

Exosomal miR-145 and miR-885 Regulate Thrombosis in COVID-19

“…Consistent with our findings, other investigators have emphasized the importance of miRs and other non-coding RNAs in the management of COVID-19 patients (Amini-Farsani et al, 2021;Battaglia et al, 2021;Dash et al, 2021;Farr et al, 2021;Lukiw, 2021;Narozna and Rubis, 2021;Plowman and Lagos, 2021;Saha et al, 2021).…”

Differential Co-Expression Network Analysis Reveals Key Hub-High Traffic Genes as Potential Therapeutic Targets for COVID-19 Pandemic

“…The inflammation regulator NFKB1 was significantly upregulated in response to SARS-CoV-2 infection; transcriptomic studies revealed its key role in regulation of differentially expressed genes (DEGs) between healthy individuals and patients with mild or severe COVID-19 (7,10,(132)(133)(134)(135)(136). Furthermore, by targeting NFKB1, miR-9 regulates inflammatory pathways related to COVID-19 pathogenesis (137). Moreover, by binding to NFKB1, miR-27a-3p suppressed NF-kB activation and reduced acute lung injury in an animal model (138).…”

Towards Personalized Medicine in Myasthenia Gravis: Role of Circulating microRNAs miR-30e-5p, miR-150-5p and miR-21-5p

“…One of our hypotheses is that the ongoing COVID-19 pandemic, which was in the middle of its 3rd peak in Sweden during serum sample collection, could have influenced the expression of our target miRNAs. As previously mentioned, miR-21-5p and miR-30e-5p levels have been shown to be increased both intracellularly and into exosomes by upregulation of the NF-kB pathway through stimulation with lipopolysaccharide [ 27 ], therefore, dysregulation of this pathway provides a theoretical link to innate immunity and to SARS-CoV-2 infection specifically [ 40 ]. Moreover, changes in miRNA expression have been proposed to happen due to infectious stimuli [ 6 ] and MG as well as the diseases included in the OND group, excluding LEMS, which is a well described paraneoplastic syndrome, have all been postulated to possibly originate from a remote viral infection [ 6 , 41 , 42 ].…”