The anti-inflammatory effects of CTS against OVA-induced airway remodeling may be through inhibiting STAT3, which further suppresses TWEAK and TGF-β1 signaling cross talk in asthma.
CONCLUSIONS Our results suggest that the therapeutic effects of DHA on asthma are partially realized via the regulation of miR-183C and IL-6/Stat3 pathway.
MiR-590-5p inhibits proliferation of fetal ASM cells by down-regulating STAT3, thereby suggesting a novel therapeutic target for the treatment of pediatric asthma.
In conclusion, we provided evidence that endogenous STAT3 mediates the pro-angiogenic ability of ASM cells by directly activating VEGF signalling, which could represent a possible therapeutic target for asthma.
Collectively, this study directly proved that STAT3 was correlated with cytokine expression in PBMCs from asthma patients, providing a potential linkage between STAT3 and pathogenesis of asthma.
We identified a significant association between STAT3 polymorphism and asthma susceptibility in atopic asthma (P < .001), whereas no such association was observed in the non-atopic asthma group (P = .9).
Furthermore, IL-6 is under the influence of the Socs3 gene and may contribute to the negative regulation of Stat3 via IL-6 following a challenge with an allergen during the development of asthma.