Camurati-Engelmann disease (CED [MIM 131300]), or progressive diaphyseal dysplasia, is an autosomal dominant sclerosing bone dysplasia characterized by progressive bone formation along the periosteal and endosteal surfaces at the diaphyseal and metaphyseal regions of long bones and cranial hyperostosis, particularly at the skull base.
In summary, PD29 reversed EMT and transformation of fibroblasts into myofibroblasts <i>in vitro</i> and prevented PF <i>in vivo</i> possibly by suppressing the TGF-β1/Smad pathway.
Here, we found that LSD1 expression was elevated in lung tissues of mice with bleomycin-induced pulmonary fibrosis and lung fibroblasts treated with transforming growth factor-β1 (TGF-β1).
GHK-Cu presented a protective effect in BLM-induced inflammation and oxidative stress by inhibiting EMT progression and suppressing TGFβ1/Smad2/3 signalling in pulmonary fibrosis.
Here, we assessed whether TGF-β1 affects the ability of HASM cells to relax in response to β<sub>2</sub>-agonists, a mainstay treatment for airway hyperresponsiveness in asthma.
Among elderly asthmatics, subjects with severe asthma had lower FEV1 (% predicted) value, but showed significantly higher serum levels of eotaxin-2 and TGF-β1, than those with non-severe asthma (<i>P</i> < 0.05 for each).
Taken together, the present results have revealed that PCA inhibits asthma airway remodeling by suppressing proliferation and extracellular matrix (ECM) protein deposition in TGF-β1-mediated ASMCs via the inactivation of Smad2/3 signaling pathway.
MicroRNA-744 Inhibits Proliferation of Bronchial Epithelial Cells by Regulating Smad3 Pathway via Targeting Transforming Growth Factor-β1 (TGF-β1) in Severe Asthma.
In the current study, we found that miR-448-5p was dramatically decreased in lung tissues of asthmatic mice and TGF-β1-stimulated bronchial epithelial cells.
Cryptotanshinone Attenuates Airway Remodeling by Inhibiting Crosstalk Between Tumor Necrosis Factor-Like Weak Inducer of Apoptosis and Transforming Growth Factor Beta 1 Signaling Pathways in Asthma.
It will further review the evidence demonstrating the extent to which IL-17A interacts with various immune factors, specifically TGF-β1, to contribute to ASM remodeling and altered function in T<sub>H</sub>17-driven endotypes of severe asthma.
The exhaled-TGF-β1 levels were significantly lower in those children with asthma exacerbation when compared to the stable asthmatic children (<i>p</i> = 0.0003).<b>Conclusion:</b> Our results suggest that TGF-β1 may play a role in suppressing airway reactivity and its deficiency is associated with asthma exacerbation.AbbreviationsACTAsthma control testAHRAirway hyper-reactivityASMAirway smooth muscleBALBronchoalveolar lavageELISAEnzyme-linked immunoassayEIBExercise-induced bronchospasmEBCExhaled breath condensateFEV1Forced expiratory volume in the first secondFEV1/FVCForced expiratory volume in the first second/forced vital capacityFEF25%-75%Forced expiratory flow, midexpiratory phaseGINAGlobal Initiative for Asthma(Ig)EImmunoglobulin EISAACInternational Study of Asthma and Allergies in ChildhoodIQRInterquartile rangeIL-10Interleukin-10TGF-β1Transforming growth factor-β1Treg cellsT regulatory cells.