ArticleAmerican journal of respiratory cell and molecular biology2019
Mitogen-activated Protein Kinase-activated Protein Kinase 2 Inhibition Attenuates Fibroblast Invasion and Severe Lung Fibrosis.
Article in American journal of respiratory cell and molecular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- Neuropsychiatric disorders in pulmonary fibrosis: from brain network alterations to inflammatory mechanisms and therapeutic implications.Journal of neuroinflammation · 2026Review
- Loading of therapeutic cell penetrating peptides into extracellular vesicles for pulmonary fibrosis.Journal of controlled release : official journal of the Controlled Release Society · 2026Article
- Protein kinase C θ deletion ameliorates bleomycin-induced pulmonary fibrosis via the improvement of SIRT1/AMPK signaling on autophagy and senescence.Iranian journal of basic medical sciences · 2026Article
- Article
- Targeted degradation of MK2 is insufficient to block inflammatory cytokine production in human cells due to cooperativity with MK3 and MK5.Frontiers in immunology · 2025Article
- Study on the efficacy of early treatment with pirfenidone on the lung function of patients with idiopathic pulmonary fibrosis.World journal of clinical cases · 2024Article
- Arrestin beta 1 Regulates Alveolar Progenitor Renewal and Lung Fibrosis.Journal of respiratory biology and translational medicine · 2024Article
- IRAK-M Regulates Proliferative and Invasive Phenotypes of Lung Fibroblasts.Inflammation · 2023Article
- Hyaluronan in the pathogenesis of acute and post-acute COVID-19 infection.Matrix biology : journal of the International Society for Matrix Biology · 2023Review
- The ZIP8/SIRT1 axis regulates alveolar progenitor cell renewal in aging and idiopathic pulmonary fibrosis.The Journal of clinical investigation · 2022Article
- Mitogen-activated protein kinase-activated protein kinase-2 (MK2) and its role in cell survival, inflammatory signaling, and migration in promoting cancer.Molecular carcinogenesis · 2022Article
- GANE can Improve Lung Fibrosis by Reducing Inflammation via Promoting p38MAPK/TGF-β1/NF-κB Signaling Pathway Downregulation.ACS omega · 2022Article
- PM2.5 Exposure Induces Lung Injury and Fibrosis by Regulating FerroptosisDisease markers · 2022Article
- Targeting Growth Factor and Cytokine Pathways to Treat Idiopathic Pulmonary Fibrosis.Frontiers in pharmacology · 2022Review
- Pathophysiological Roles of Stress-Activated Protein Kinases in Pulmonary Fibrosis.International journal of molecular sciences · 2021Review
- Therapeutic targeting of argininosuccinate synthase 1 (ASS1)-deficient pulmonary fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Transcriptomic Evaluation of Pulmonary Fibrosis-Related Genes: Utilization of Transgenic Mice with Modifying p38 Signal in the Lungs.International journal of molecular sciences · 2020Article
- Update in Interstitial Lung Disease 2019.American journal of respiratory and critical care medicine · 2020Review
- Cardiac Fibroblast p38 MAPK: A Critical Regulator of Myocardial Remodeling.Journal of cardiovascular development and disease · 2019Review
- MMI-0100 Ameliorates Dextran Sulfate Sodium-Induced Colitis in Mice through Targeting MK2 Pathway.Molecules (Basel, Switzerland) · 2019Article
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Severe pulmonary fibrosis such as idiopathic pulmonary fibrosis (IPF) is characterized by the accumulation of extracellular matrix and fibroblast activation. Targeting fibroblast activation has contributed to the development of antifibrotic therapeutics for patients with IPF. Mitogen-activated protein kinase-activated protein kinase 2 (MK2), downstream in the transforming growth factor-β/p38 mitogen-activated protein kinase pathway, has been implicated in inflammatory and fibrosing diseases. Increased concentrations of activated MK2 were expressed in IPF lung and in the mouse bleomycin model of lung fibrosis. The aim of the present study was to determine the role and the mechanisms of MK2 in fibroblast invasion and lung fibrosis. Our results showed that an MK2 inhibitor (MMI-0100) was able to inhibit the invasive capacity of lung fibroblasts isolated from patients with IPF, as well as fibroblasts isolated from both wild-type mice and mice with overexpressing hyaluronan synthase 2 (HAS2) in the myofibroblast compartment. We previously showed that hyaluronan and HAS2 regulate fibroblast invasion and lung fibrosis in vivo. The results of the present study showed that MMI-0100 reduced transforming growth factor-β-induced hyaluronan production in human and mouse fibroblasts in vitro and that HAS2 mediated MK2 activation, suggesting a feed-forward loop in fibroblast activation. More importantly, MK2 inhibition attenuated hyaluronan accumulation and reduced collagen content in bleomycin-injured mouse lungs in vivo. Conditional deletion of MK2 in fibroblasts attenuated bleomycin-induced lung fibrosis. These data provide evidence that MK2 has a role in fibroblast invasion and fibrosis and may be a novel therapeutic target in pulmonary fibrosis.
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