2018
DOI: 10.1016/j.intimp.2017.12.010
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Interleukin-37 alleviates airway inflammation and remodeling in asthma via inhibiting the activation of NF-κB and STAT3 signalings

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Cited by 55 publications
(31 citation statements)
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“…Myofibroblasts express α-SMA, which mediate the contractile activity of fibroblastic cells, in addition to their production of collagen types I, III, IV and V [97]. Moreover, TGF-β1 increases contractility, migration and proliferation of airway smooth muscle cells [95,98]. Therefore, it is not surprising that TGF-β1 correlates with the airway narrowing and limitation of air movements in asthmatic patients [91].…”
Section: Tgf-β1mentioning
confidence: 99%
“…Myofibroblasts express α-SMA, which mediate the contractile activity of fibroblastic cells, in addition to their production of collagen types I, III, IV and V [97]. Moreover, TGF-β1 increases contractility, migration and proliferation of airway smooth muscle cells [95,98]. Therefore, it is not surprising that TGF-β1 correlates with the airway narrowing and limitation of air movements in asthmatic patients [91].…”
Section: Tgf-β1mentioning
confidence: 99%
“…Higher level of activated NF-κB is observed in asthma, various strategies targeting NF-κB signaling have been considered for asthma treatment [22]. STAT3 is an important transcription factor that has been found to be implicated in airway inflammation and remodeling in asthma [23]. Jeon et al [8] reported that eupatilin inhibits NF-κB signaling in bronchial epithelial cells, leading to inhibition of eosinophil migration.…”
Section: Discussionmentioning
confidence: 99%
“…The levels of in ammation and brosis in the STAT3-siRNA group were signi cantly reduced compared with that in the RHD group. STAT3 is also involved in many diseases, such as airway in ammation and rheumatoid arthritis [32][33][34][35]. The persistent activation and high expression of STAT3 in tumour cells promotes tumour growth and proliferation [7].…”
Section: Discussionmentioning
confidence: 99%