Though the exact pathophysiological mechanisms of IPF remain unknown, TGF-β1 is thought to act as a main driver of the disease by mediating fibroblast-to-myofibroblast transformation (FMT). Recent reports have indicated that a metabolic shift towards aerobic glycolysis takes place during FMT and ...
Madeja ZbigniewSpringer International PublishingCellular & Molecular Life SciencesMichalik, M.; Wojcik-Pszczoła, K.; Paw, M.; Wnuk, D.; Koczurkiewicz, P.; Sanak, M.; Pe˛kala, E.; Madeja, Z. Fibroblast-to-myofibroblast transition in bronchial asthma. Cell. Mol. Life Sci. 2018. [...
Vol.:01345678913CellularandMolecularLifeSciences01875:3943–3961https://doi.org/10.1007/s00018-018-899-4REVIEWFibroblast‑to‑myofibroblasttransitionin bronchialasthmaMarta Michalik1 ·Katarzyna Wójcik‑Pszczoła1 ·Milena Paw1 ·Dawid Wnuk1 ·P
Human bronchial fibroblasts (HBFs) derived from patients diagnosed with asthma display in vitro predestination towards TGF-β-induced fibroblast-to-myofibroblast transition (FMT), a key event in subepithelial fibrosis. As commonly used anti-asthmatic drugs do not reverse the structural changes of the ...
In response to tissue injury, these cells undergo a dynamic fibroblast–myofibroblast transition, marked by extracellular matrix secretion and contraction of actomyosin-based stress fibres. Importantly, whereas transient activation into myofibroblasts aids in tissue repair, persistent activation triggers ...
Background Fibroblast to myofibroblast transition is believed to contribute to airway remodelling in lung diseases such as asthma and chronic obstructive pulmonary disease. This study examines the role of aclidinium, a new long-acting muscarinic antagonist, on human fibroblast to myofibroblast transition....
STAT-3 contributes to pulmo- nary fibrosis through epithelial injury and fibro- blast-myofibroblast differentiation. FASEB J 2016; 30: 129-140.Pedroza M, Le TT, Lewis K, Karmouty-Quintana H, To S, George AT, Blackburn MR, Tweardy DJ, Agarwal SK. STAT-3 contributes to pulmonary ...
Objective:To study whether PPAR-γ agonist rosiglitazone could inhibit fibronectin -induced pulmonary fibroblast to myofibroblast transition and its possible mechanism.Methods:Pulmonary fibroblasts are cultured in a Petri dish coated with Fn.The expression of related proteins was detected by immunocytochemistry...
Programmed death ligand-1 (PD-L1) is an immune checkpoint protein that has been linked with idiopathic pulmonary fibrosis (IPF) and fibroblast to myofibroblast transition (FMT). However, it remains largely unclear how PD-L1 mediates this process. We found significantly increased PD-L1 in the lun...
Myofibroblasts predominantly emerging through fibroblast-to-myofibroblast transition (FMT) are considered to be the key collagen-producing cells in pulmonary fibrosis. Circular RNAs (circRNAs) are important players involved in many biological processes. circHIPK3 has been identified as the one of the mo...