ArticleAdvances in bioscience and biotechnology (Print)2019
Constitutive AKT Activity Predisposes Lung Fibrosis by Regulating Macrophage, Myofibroblast and Fibrocyte Recruitment and Changes in Autophagy.
Article in Advances in bioscience and biotechnology (Print), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Article
- Protein lipidation in the tumor microenvironment: enzymology, signaling pathways, and therapeutics.Molecular cancer · 2025Review
- Insights into CSF-1/CSF-1R signaling: the role of macrophage in radiotherapy.Frontiers in immunology · 2025Review
- Zanubrutinib Ameliorates Cardiac Fibrosis and Inflammation Induced by Chronic Sympathetic Activation.Molecules (Basel, Switzerland) · 2023Article
- Treprostinil Reconstitutes Mitochondrial Organisation and Structure in Idiopathic Pulmonary Fibrosis Cells.International journal of molecular sciences · 2023Article
- Autophagy in pulmonary fibrosis: friend or foe?Genes & diseases · 2022Article
- Article
- TSSK4 upregulation in alveolar epithelial type-II cells facilitates pulmonary fibrosis through HSP90-AKT signaling restriction and AT-II apoptosis.Cell death & disease · 2021Article
- Antifibrotic and Regenerative Effects of Treamid in Pulmonary Fibrosis.International journal of molecular sciences · 2020Article
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Authors and funding
8 authors.
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Abstract
The etiology and pathogenesis of pulmonary fibrosis is poorly understood. We and others reported that M-CSF/CSF-1, M-CSF-R and downstream AKT activation plays an important role in lung fibrosis in mice models and in IPF patients. To understand potential molecular pathways used by M-CSF-R activation to direct lung fibrosis, we used a novel transgenic mouse model that expresses a constitutively-active form of AKT, myristoylated AKT (Myr-Akt), driven by the
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