ArticleOncotarget2016
Redox-sensitive MAPK and Notch3 regulate fibroblast differentiation and activation: a dual role of ERK1/2.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Branched-chain amino acid transaminase 1-mediated pathway promotes proline-dependent collagen production in cardiac myofibroblasts.The Journal of clinical investigation · 2026Article
- The Complex Interplay of TGF-β and Notch Signaling in the Pathogenesis of Fibrosis.International journal of molecular sciences · 2024Review
- Selenium deficiency-induced multiple tissue damage with dysregulation of immune and redox homeostasis in broiler chicks under heat stress.Science China. Life sciences · 2023Article
- The emerging role of NOTCH3 receptor signalling in human lung diseases.Expert reviews in molecular medicine · 2022Review
- Exploring the Anti-Pulmonary Fibrosis Mechanism of Jingyin Granule by Network Pharmacology Strategy.Frontiers in pharmacology · 2022Article
- DNA Methyltransferase 1 Is Dysregulated in Parkinson's Disease via Mediation of miR-17.Molecular neurobiology · 2021Article
- Idiopathic Pulmonary Comorbidities and Mechanisms.International journal of inflammation · 2021Review
- Molecular determinants of mesenchymal cell activation in fibroproliferative diseases.Cellular and molecular life sciences : CMLS · 2019Review
- Identifying miRNA-mRNA regulation network of chronic pancreatitis based on the significant functional expression.Medicine · 2017Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myofibroblastic transformation, characterized by upregulation of α-smooth muscle actin in response to proï¬brotic agents such as TGF-β1, is considered as a major event leading to ï¬brosis. The mechanistic basis linking myoï¬broblast differentiation to idiopathic pulmonary ï¬brosis and the disease treatment remain elusive. In this study, we studied roles of MAPK, Notch, and reactive oxygen species (ROS) during the differentiation of IMR-90 lung fibroblasts at basal level and induced by TGF-β1. Our results demonstrated that ROS-dependent activation of p38, JNK1/2 and Notch3 promoted basal and TGF-β1-induced differentiation and expression of extracellular matrix proteins. In stark contrast, ERK1/2 was suppressed by ROS and exhibited an inhibitory effect on the differentiation but showed a weak promotion on the expression of extracellular matrix proteins. TGF-β1-induced Notch3 expression depended on p38 and JNK1/2. Interestingly, Notch3 was also downstream of ERK1/2, suggesting a complex role of ERK1/2 in lung function. Our results suggest a novel ROS-mediated shift of dominance from the inhibitory ERK1/2 to the stimulatory p38, JNK1/2 and Notch3 during the pathological progression of IPF. Thus, targeting ERK1/2 signaling for activation and p38, JNK1/2 and Notch3 for inhibition may be of clinical potential against lung fibrosis.
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