ArticlePloS one2015
IL-13 induces YY1 through the AKT pathway in lung fibroblasts.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Fibroblast-centered mechanisms of chronic inflammation and airway remodeling in allergic bronchopulmonary aspergillosis.Frontiers in allergy · 2026Review
- Pathogenic group 2 innate lymphoid cells as drivers of lung fibrosis in severe asthma.Frontiers in immunology · 2026Review
- Idiopathic Pulmonary Fibrosis Caused by Damaged Mitochondria and Imbalanced Protein Homeostasis in Alveolar Epithelial Type II Cell.Advanced biology · 2025Review
- ST2L promotes VEGFA-mediated angiogenesis in gastric cancer by activating TRAF6/PI3K/Akt/NF-κB pathway via IL-33.Scientific reports · 2024Article
- Specific epigenetic regulators serve as potential therapeutic targets in idiopathic pulmonary fibrosis.Heliyon · 2022Review
- Role of interleukins in the pathogenesis of pulmonary fibrosis.Cell death discovery · 2021Review
- Cardioprotective Roles of Endothelial Progenitor Cell-Derived Exosomes.Frontiers in cardiovascular medicine · 2021Review
- The Epithelial-Immune Crosstalk in Pulmonary Fibrosis.Frontiers in immunology · 2021Review
- The Effect of Nintedanib on T-Cell Activation, Subsets and Functions.Drug design, development and therapy · 2021Article
- Exogenous miR-29a Attenuates Muscle Atrophy and Kidney Fibrosis in Unilateral Ureteral Obstruction Mice.Human gene therapy · 2020Article
- FAM3C-YY1 axis is essential for TGFβ-promoted proliferation and migration of human breast cancer MDA-MB-231 cells via the activation of HSF1.Journal of cellular and molecular medicine · 2019Article
- Exosome-Mediated miR-29 Transfer Reduces Muscle Atrophy and Kidney Fibrosis in Mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2019Article
- The Two Sides of YY1 in Cancer: A Friend and a Foe.Frontiers in oncology · 2019Review
- miR‑29a suppresses IL‑13‑induced cell invasion by inhibiting YY1 in the AKT pathway in lung adenocarcinoma A549 cells.Oncology reports · 2018Article
- Deciphering the pathways that protect from IL-13-mediated potentiation of oxidative stress-induced dopaminergic nerve cell death.Cytokine · 2018Article
- The Selective Angiotensin II Type 2 Receptor Agonist, Compound 21, Attenuates the Progression of Lung Fibrosis and Pulmonary Hypertension in an Experimental Model of Bleomycin-Induced Lung Injury.Frontiers in physiology · 2018Article
- Insulin signaling via the PI3-kinase/Akt pathway regulates airway glucose uptake and barrier function in a CFTR-dependent manner.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- Interleukin-13 and age-related macular degeneration.International journal of ophthalmology · 2017Article
- Nicotine Suppressed Fetal Adrenal StAR Expression via YY1 Mediated-Histone Deacetylation Modification Mechanism.International journal of molecular sciences · 2016Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
A key feature of lung fibrosis is the accumulation of myofibroblasts. Interleukin 13 (IL-13) is a pro-fibrotic mediator that directly and indirectly influences the activation of myofibroblasts. Transforming growth factor beta (TGF-β) promotes the differentiation of fibroblasts into myofibroblasts, and can be regulated by IL-13. However, IL-13's downstream signaling pathways are not completely understood. We previously reported that the transcription factor Yin Yang 1 (YY1) is upregulated in fibroblasts treated with TGF-β and in the lungs of mice and patients with pulmonary fibrosis. Moreover, YY1 directly regulates collagen and alpha smooth muscle actin (α-SMA) expression in fibroblasts. However, it is not known if IL-13 regulates fibroblast activation through YY1 expression. We hypothesize that IL-13 up-regulates YY1 expression through regulation of AKT activation, leading to fibroblast activation. In this study we found that YY1 was upregulated by IL-13 in lung fibroblasts in a dose- and time-dependent manner, resulting in increased α-SMA. Conversely, knockdown of YY1 blocked IL-13-induced α-SMA expression in fibroblasts. Furthermore, AKT phosphorylation was increased in fibroblasts treated with IL-13, and AKT overexpression upregulated YY1, whereas blockade of AKT phosphorylation suppressed the induction of YY1 by IL-13 in vitro. In vivo YY1 was upregulated in fibrotic lungs from CC10-IL-13 transgenic mice compared to that from wild-type littermates, which was associated with increased AKT phosphorylation. Taken together, these findings demonstrate that IL-13 is a potent stimulator and activator of fibroblasts, at least in part, through AKT-mediated YY1 activation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.