ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2019
Tackling MARCKS-PIP3 circuit attenuates fibroblast activation and fibrosis progression.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- Folate metabolism-related gene signature reveals prognostic and immunological characteristics in idiopathic pulmonary fibrosis.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2026Article
- Identification of a small-molecule targeting PLAGL2 DNA-binding domain inhibits extracellular matrix formation and enhances lenvatinib sensitivity in hepatocellular carcinoma.Acta pharmaceutica Sinica. B · 2026Article
- Repurposing flavopiridol as an inhaled therapeutic for pulmonary fibrosis.European journal of pharmacology · 2025Article
- MARCKS N-terminal sequence-derived inhibitor peptides impair monocytic ROS production and migration via MARCKS-independent effects.Molecular biology reports · 2025Article
- Dapagliflozin Suppresses High Glucose-Induced Proliferation, Oxidative Stress, and Fibrosis by Reducing Mettl3-Induced m6A Modification in Marcks mRNA.Cardiovascular toxicology · 2025Article
- Transcriptomics in idiopathic pulmonary fibrosis unveiled: a new perspective from differentially expressed genes to therapeutic targets.Frontiers in immunology · 2024Article
- TGF-β1 overexpression in severe COVID-19 survivors and its implications for early-phase fibrotic abnormalities and long-term functional impairment.Frontiers in immunology · 2024Article
- A myristoylated alanine-rich C-kinase substrate (MARCKS) inhibitor peptide attenuates neutrophil outside-in βCell adhesion & migration · 2023Article
- Inositol possesses antifibrotic activity and mitigates pulmonary fibrosis.Respiratory research · 2023Article
- Metformin attenuates fibroblast activation during pulmonary fibrosis by targeting S100A4Frontiers in pharmacology · 2023Article
- MARCKS Is an Essential Regulator of Reactive Oxygen Species Production in the Monocytic Cell Type.Antioxidants (Basel, Switzerland) · 2022Article
- The Combined Model of CX3CR1-Related Immune Infiltration Genes to Evaluate the Prognosis of Idiopathic Pulmonary Fibrosis.Frontiers in immunology · 2022Article
- A Novel Renoprotective Strategy: Upregulation of PD-L1 Mitigates Cisplatin-Induced Acute Kidney Injury.International journal of molecular sciences · 2021Article
- Targeting the AXL Receptor in Combating Smoking-related Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2021Article
- Therapeutic targeting of argininosuccinate synthase 1 (ASS1)-deficient pulmonary fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- MARCKS cooperates with NKAP to activate NF-kB signaling in smoke-related lung cancer.Theranostics · 2021Article
- Gypenosides Attenuate Pulmonary Fibrosis by Inhibiting the AKT/mTOR/c-Myc Pathway.Frontiers in pharmacology · 2021Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Targeting activated fibroblasts, including myofibroblast differentiation, has emerged as a key therapeutic strategy in patients with idiopathic pulmonary fibrosis (IPF). However, there is no available therapy capable of selectively eradicating myofibroblasts or limiting their genesis. Through an integrative analysis of the regulator genes that are responsible for the activation of IPF fibroblasts, we noticed the phosphatidylinositol 4,5-bisphosphate (PIP2)-binding protein, myristoylated alanine-rich C-kinase substrate (MARCKS), as a potential target molecule for IPF. Herein, we have employed a 25-mer novel peptide, MARCKS phosphorylation site domain sequence (MPS), to determine if MARCKS inhibition reduces pulmonary fibrosis through the inactivation of PI3K/protein kinase B (AKT) signaling in fibroblast cells. We first observed that higher levels of MARCKS phosphorylation and the myofibroblast marker α-smooth muscle actin (α-SMA) were notably overexpressed in all tested IPF lung tissues and fibroblast cells. Treatment with the MPS peptide suppressed levels of MARCKS phosphorylation in primary IPF fibroblasts. A kinetic assay confirmed that this peptide binds to phospholipids, particularly PIP2, with a dissociation constant of 17.64 nM. As expected, a decrease of phosphatidylinositol (3,4,5)-trisphosphate pools and AKT activity occurred in MPS-treated IPF fibroblast cells. MPS peptide was demonstrated to impair cell proliferation, invasion, and migration in multiple IPF fibroblast cells
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