ArticleThe international journal of biochemistry & cell biology2012
Survivin expression induced by endothelin-1 promotes myofibroblast resistance to apoptosis.
Article in The international journal of biochemistry & cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 79 citations in OpenAlex.
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- Development of a high-throughput TR-FRET assay to identify inhibitors of the FAK-paxillin protein-protein interaction.SLAS discovery : advancing life sciences R & D · 2025Article
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- A novel senolytic drug for pulmonary fibrosis: BTSA1 targets apoptosis of senescent myofibroblasts by activating BAX.Aging cell · 2024Article
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- Survivin as a mediator of stiffness-induced cell cycle progression and proliferation of vascular smooth muscle cells.APL bioengineering · 2023Article
- Towards a Unified Approach in Autoimmune Fibrotic Signalling Pathways.International journal of molecular sciences · 2023Review
- p53 and Myofibroblast Apoptosis in Organ Fibrosis.International journal of molecular sciences · 2023Review
- Regulation of Mesenchymal Cell Fate by Transfer of Active Gasdermin-D via Monocyte-Derived Extracellular Vesicles.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Mechanical homeostasis imbalance in hepatic stellate cells activation and hepatic fibrosis.Frontiers in molecular biosciences · 2023Review
- Angiogenic gene characterization and vessel permeability of dermal microvascular endothelial cells isolated from burn hypertrophic scar.Scientific reports · 2022Article
- Bortezomib Inhibits Lung Fibrosis and Fibroblast Activation without Proteasome Inhibition.American journal of respiratory cell and molecular biology · 2022Article
- The NaCellular and molecular life sciences : CMLS · 2021Review
- Myofibroblast fate plasticity in tissue repair and fibrosis: Deactivation, apoptosis, senescence and reprogramming.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society · 2021Article
- A novel tree shrew model of pulmonary fibrosis.Laboratory investigation; a journal of technical methods and pathology · 2021Article
- Why Stress Matters: An Introduction.Methods in molecular biology (Clifton, N.J.) · 2021Review
- You Say You Want a Resolution (of Fibrosis).American journal of respiratory cell and molecular biology · 2020Review
- Mechano-therapeutics: Targeting Mechanical Signaling in Fibrosis and Tumor Stroma.Pharmacology & therapeutics · 2020Review
- ET-1 promotes the growth and metastasis of esophageal squamous cell carcinoma via activating PI3K/Akt pathway.Translational cancer research · 2020Article
- Evasion of apoptosis by myofibroblasts: a hallmark of fibrotic diseases.Nature reviews. Rheumatology · 2020Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Fibrosis of the lungs and other organs is characterized by the accumulation of myofibroblasts, effectors of wound-repair that are responsible for the deposition and organization of new extracellular matrix (ECM) in response to tissue injury. During the resolution phase of normal wound repair, myofibroblast apoptosis limits the continued deposition of ECM. Mounting evidence suggests that myofibroblasts from fibrotic wounds acquire resistance to apoptosis, but the mechanisms regulating this resistance have not been fully elucidated. Endothelin-1 (ET-1), a soluble peptide strongly associated with fibrogenesis, decreases myofibroblast susceptibility to apoptosis through activation of phosphatidylinositol 3'-OH kinase (PI3K)/AKT. Focal adhesion kinase (FAK) also promotes myofibroblast resistance to apoptosis through PI3K/AKT-dependent and -independent mechanisms, although the role of FAK in ET-1 mediated resistance to apoptosis has not been explored. The goal of this study was to investigate whether FAK contributes to ET-1 mediated myofibroblast resistance to apoptosis and to examine potential mechanisms downstream of FAK and PI3K/AKT by which ET-1 regulates myofibroblast survival. Here, we show that ET-1 regulates myofibroblast survival by Rho/ROCK-dependent activation of FAK. The anti-apoptotic actions of FAK are, in turn, dependent on activation of PI3K/AKT and the subsequent increased expression of Survivin, a member of the inhibitor of apoptosis protein (IAP) family. Collectively, these studies define a novel mechanism by which ET-1 promotes myofibroblast resistance to apoptosis through upregulation of Survivin.
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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.