| MiR-494 |
NAD(P)H: quinone oxidoreductase 1 (NQO1); |
In a rat model of sepsis-associated ARDS, the up-regulation of miR-494 decreased the expression of the antioxidant factor NQO1 and inactivated the Nrf2 signaling pathway, which were responsible for significantly higher levels of IL-1β, IL-6, and TNF-α, suggesting a pro-inflammatory effect of miR-494 on sepsis-associated ARDS [48]. |
| miR-199a |
Sirtuin1(SIRT1) |
MicroRNA-199a (miR-199a) exerted a protective effect on sepsis-induced ARDS and was negatively correlated with SIRT1 expression. The down-regulation of miR-199a up-regulated SIRT1 expression, which suppressed excessive inflammatory responses and inhibited cellular apoptosis in subjects with sepsis-induced ARDS [50]. |
| Jun N-terminal kinase (JNK) and p38 |
Mitogen-activated protein kinase (MAPK) signal |
MAPK signaling is suppressed by blocking the phosphorylation of JNK and p38, which decreases the levels of the pro-inflammatory cytokines IL-6 and TNF-α and increases the level of the anti-inflammatory cytokine IL-10 to subsequently alleviate the inflammation in subjects with sepsis-induced ARDS [54]. |
| RNFT2 |
IL-3Rα |
RNFT2 decreases the expression of IL-3Rα by targeting it for proteasomal degradation after inducing its ubiquitination at Lys357, which inhibited pro-inflammatory cytokine and immune cell release in rats' lung inflammation models [55]. |
| LincRNA-p21 |
Thy-1 (CD90) |
The overexpression of lincRNA-p21 inhibits Thy-1 expression by inhibiting the acetylation of H3 and H4 at the Thy-1 promoter and remarkably suppressing the expression of the Thy-1 mRNA, which promotes the proliferation of the human lung fibroblasts cell line HLF1 [49]. |
