Table 2.
Human top ranked miRs expression in lung during COVID-19 progression.
| miR | Target gene | Up/down Regulation | Effect |
|---|---|---|---|
| miR-8066 |
-PRLR, CXCL6, IL6, IL17, IL10 and ACVR1 -TGF-β pathway, mucin type O-Glycan and cytokine-cytokine receptor interaction -chemokine binding receptors - FGFR pathway |
Up | -Activate NfKB to target pro-inflammatory cytokines and induce cytokine storm -Increased NfKB mediated TLR-8 expression -Change N-glycosylation patterns -Upregulation of FGFR pathways |
| miR-5197–3p | TGF-β, mucin type O-Glycan and cytokine-cytokine receptor interaction | Up | -Similar to miR-8066 -And also GABAergic synapse, morphine addiction and metabolism of xenobiotics by cytochrome P450 |
| miR-3611 | GABAergic synapse, morphine addiction and metabolism of xenobiotics by cytochrome P450 | Down | -Probably promote viral replication |
| miR-1468–5p | TGF-1 and MAPKs signalling | Up | -Cardiac fibrosis |
| miR-1307–3p | TGF-β and semaphorin signalling | Up | -Promote inflammatory responses |
| miR-3691–3p | TGF-signalling, FGF2 and VCAM1 | Down | -Lung pathogenesis |
| miR-3934–3p | TGFBR1 and SMAD3 | Down | -Affect glycosaminoglycan biosynthesis-heparan sulfate/heparin, other types of O-glycan biosynthesis and vitamin digestion-absorption mechanisms |